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  • 1.
    Ahn, Henrik Casimir
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Thoracic Surgery. Östergötlands Läns Landsting, Heart Centre, Department of Thoracic and Vascular Surgery.
    Lindhagen, J
    Nilsson, Gert
    Linköping University, The Institute of Technology. Linköping University, Department of Biomedical Engineering, Biomedical Instrumentation.
    Salerud, Göran
    Linköping University, The Institute of Technology. Linköping University, Department of Biomedical Engineering, Biomedical Instrumentation.
    Jodal, M
    Lundgren, O
    Evaluation of Laser Doppler Flowmetry in the assessment of intestinal blood flow1985In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 4, no 88, p. 951-957Article in journal (Refereed)
    Abstract [en]

      

  • 2. Andersson, Roland
    et al.
    Olaison, Gunnar
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Surgery. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Surgery in Östergötland.
    Tysk, Curt
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Gastroenterology and Hepatology.
    Ekbom, Anders
    Appendectomy is followed by increased risk of Crohn's disease2003In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 124, no 1, p. 40-46Article in journal (Refereed)
    Abstract [en]

    Background & Aims: Appendectomy is associated with a low risk of subsequent ulcerative colitis. This study analyzes the risk of Crohn's disease after appendectomy. Methods: We followed-up 212,218 patients with appendectomy before age 50 years and a cohort of matched controls, identified from the Swedish Inpatient Register and the nationwide Census, for any subsequent diagnosis of Crohn's disease. Results: An increased risk of Crohn's disease was found for more than 20 years after appendectomy, with incidence rate ratio 2.11 (95% confidence interval [CI], 1.21-3.79) after perforated appendicitis, 1.85 (95% CI, 1.10-3.18) after nonspecific abdominal pain, 2.15 (95% CI, 1.25-3.80) after mesenteric lymphadenitis, 2.52 (95% CI, 1.43-4.63) after other diagnoses. After nonperforated appendicitis, there was an increased risk among women but not among men (incidence rate ratio 1.37, 95% CI, 1.03-1.85, respectively, 0.89, 95% CI, 0.64-1.24). Patients operated on before age 10 years had a low risk (incidence rate ratio 0.48, 95% CI, 0.23-0.97). Crohn's disease patients with a history of perforated appendicitis had a worse prognosis. Conclusions: Appendectomy is associated with an increased risk of Crohn's disease that is dependent on the patient's sex, age, and the diagnosis at operation. The pattern of associations suggests a biologic cause.

  • 3. Bantel, H.
    et al.
    Berg, C.
    Vieth, M. W.
    Stolte, M.
    Kruis, W.
    Luegering, N.
    Domschke, W.
    Los, Marek Jan
    Department of Immunology and Cell Biology, University of Münster, Münster, Germany.
    Schulze-Osthoff, Klaus
    Department of Immunology and Cell Biology, University of Münster, Münster, Germany .
    Mesalazine inhibits activation of transcription factor NF-KB in inflamed mucosa of patients with ulcerative colitis.2000In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 118, no 4, p. A1116-A1116Article in journal (Refereed)
  • 4.
    Bednarska, Olga
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Walter, Susanna
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Gastroentorology. Linköping University, Center for Medical Image Science and Visualization (CMIV).
    Casado-Bedmar, Maite
    Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Medicine and Health Sciences.
    Ström, Magnus
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Gastroentorology.
    Salvo-Romero, Eloisa
    University of Autonoma Barcelona, Spain.
    Vicario, Maria
    University of Autonoma Barcelona, Spain.
    Mayer, Emeran A.
    University of Calif Los Angeles, CA 90095 USA.
    Keita, Åsa
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Vasoactive Intestinal Polypeptide and Mast Cells Regulate Increased Passage of Colonic Bacteria in Patients With Irritable Bowel Syndrome2017In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 153, no 4, p. 948-+Article in journal (Refereed)
    Abstract [en]

    BACKGROUND amp; AIMS: Irritable bowel syndrome (IBS) is associated with intestinal dysbiosis and symptoms of IBS develop following gastroenteritis. We aimed to study the passage of live bacteria through the colonic epithelium, and determine the role of mast cells (MCs) and vasoactive intestinal polypeptide (VIP) in barrier regulation in IBS and healthy individuals. METHODS: Colon biopsies from 32 women with IBS and 15 age-matched healthy women (controls) were mounted in Ussing chambers; we measured numbers of fluorescently labeled Escherichia coli HS and Salmonella typhimurium that passed through from the mucosal side to the serosal side of the tissue. Some biopsies were exposed to agents that block the VIP receptors (VPAC1 and VPAC2) or MCs. Levels of VIP and tryptase were measured in plasma and biopsy lysates. Number of MCs and MCs that express VIP or VIP receptors were quantified by immunofluorescence. Biopsies from an additional 5 patients with IBS and 4 controls were mounted in chambers and Salmonella were added; we studied passage routes through the epithelium by transmission electron microscopy and expression of tight junctions by confocal microscopy. RESULTS: In colon biopsies from patients with IBS, larger numbers of E coli HS and S typhimurium passed through the epithelium than in biopsies from controls (P amp;lt;.0005). In transmission electron microscopy analyses, bacteria were found to cross the epithelium via only the transcellular route. Bacterial passage was reduced in biopsies from patients with IBS and controls after addition of antibodies against VPACs or ketotifen, which inhibits MCs. Plasma samples from patients with IBS had higher levels of VIP than plasma samples from controls. Biopsies from patients with IBS had higher levels of tryptase, larger numbers of MCs, and a higher percentage of MCs that express VPAC1 than biopsies from controls. In biopsies from patients with IBS, addition of Salmonella significantly reduced levels of occludin; subsequent addition of ketotifen significantly reversed this effect. CONCLUSIONS: We found that colonic epithelium tissues from patients with IBS have increased translocation of commensal and pathogenic live bacteria compared with controls. The mechanisms of increased translocation include MCs and VIP.

  • 5.
    Berg, Anna
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Cell Biology.
    Ericson, Ann-Charlott
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Cell Biology.
    Kechagias, Stergios
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Sjöstrand, Sven-Erik
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Pharmacology .
    Unique localization of eNOS-IR in human gastric mucosa.2000In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 118, no 4, p. 5095-Conference paper (Other academic)
  • 6.
    Bolling-Sternevald, E
    et al.
    Linkoping Univ Hosp, Dept Biomed & Surg, S-58185 Linkoping, Sweden AstraZeneca R&D, Molndal, Sweden Odense Univ Hosp, Dept Gastroenterol, DK-5000 Odense, Denmark.
    Carlsson, R
    Aalykke, C
    Linkoping Univ Hosp, Dept Biomed & Surg, S-58185 Linkoping, Sweden AstraZeneca R&D, Molndal, Sweden Odense Univ Hosp, Dept Gastroenterol, DK-5000 Odense, Denmark.
    Wilson, B
    Linkoping Univ Hosp, Dept Biomed & Surg, S-58185 Linkoping, Sweden AstraZeneca R&D, Molndal, Sweden Odense Univ Hosp, Dept Gastroenterol, DK-5000 Odense, Denmark.
    Junghard, O
    Linkoping Univ Hosp, Dept Biomed & Surg, S-58185 Linkoping, Sweden AstraZeneca R&D, Molndal, Sweden Odense Univ Hosp, Dept Gastroenterol, DK-5000 Odense, Denmark.
    Lauritsen, K
    Linkoping Univ Hosp, Dept Biomed & Surg, S-58185 Linkoping, Sweden AstraZeneca R&D, Molndal, Sweden Odense Univ Hosp, Dept Gastroenterol, DK-5000 Odense, Denmark.
    Glise, Hans
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery.
    Gastrointestinal (GI) symptoms, quality of life and endoscopic diagnoses in patients with upper GI symptoms2001In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 120, no 5, p. 1248-Conference paper (Other academic)
  • 7.
    Elmberg, M.
    et al.
    Dept. of Gastroenterol. and Hepatol., Karolinska Hospital, S-171 76 Stockholm, Sweden.
    Hultcrantz, R.
    Dept. of Gastroenterol. and Hepatol., Karolinska Hospital, S-171 76 Stockholm, Sweden.
    Ekbom, A.
    Department of Medicine, Clinical Epidemiology Unit, Karolinska Hospital, Stockholm, Sweden.
    Brandt, L.
    Department of Medicine, Clinical Epidemiology Unit, Karolinska Hospital, Stockholm, Sweden.
    Olsson, S.
    Department of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Olsson, R.
    Department of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Lindgren, S.
    Department of Medicine, Malmö University Hospital, Malmö, Sweden.
    Loof, L.
    Lööf, L., Department of Medicine, Uppsala Academic Hospital, Uppsala, Sweden.
    Stal, P.
    Department of Medicine, Danderyds Hospital, Danderyd, Sweden.
    Wallerstedt, S.
    Department of Medicine, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Almer, Sven
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Gastroenterology and Hepatology . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Sandberg-Gertzen, H.
    Sandberg-Gertzén, H., Department of Medicine, Örebro University Hospital, Örebro, Sweden.
    Askling, J.
    Department of Medicine, Clinical Epidemiology Unit, Karolinska Hospital, Stockholm, Sweden.
    Cancer Risk in Patients with Hereditary Hemochromatosis and in Their First-Degree Relatives2003In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 125, no 6, p. 1733-1741Article in journal (Refereed)
    Abstract [en]

    Background & Aims: Iron overload may be carcinogenic. Patients with hereditary hemochromatosis (HH) are reportedly at a 20-200-fold risk of intrahepatic cancer, but the reported risks for nonhepatobiliary cancers are conflicting. The risk of cancer in heterozygous individuals (estimated allele frequency, 1/10 to 1/20) is unknown. This study aimed to better assess these risks. Methods: We performed a population-based cohort study of 1847 Swedish patients with HH and 5973 of their first-degree relatives using nationwide, population-based health and census registers. We used standardized incidence ratios (SIRs) as relative risk. Results: With 62 liver cancers and 128 nonhepatobiliary cancers, patients with HH were at a 20-fold risk of liver cancer (SIR, 21, 95% confidence interval [Cl], 16-22) but an almost unaltered risk of all other cancers (SIR, 1.2, 95% Cl, 1.0-1.4), including nonelevated risks for several gastrointestinal tract cancers. At 10 years of follow-up, the absolute risk of liver cancer was 6% among men and 1.5% among women. With 21 liver cancers and 508 nonhepatobiliary cancers, first-degree relatives were at an unaltered risk of extrahepatic cancer (SIR, 1.0, 95% Cl, 0.9-1.1, including unelevated risks for gastrointestinal cancers) but at a modest and historic increased risk of hepatobiliary cancer (SIR, 1.5, 95% Cl, 1.0-2.4), the histopathologic spectrum of which differed from the patients. Conclusions: Patients (particularly men) with HH are at increased risk for hepatocellular cancer, although the magnitude of the risk is lower than previous estimates. Overall cancer risk in first-degree relatives does not seem to be increased.

  • 8.
    Everhov, Asa H.
    et al.
    Karolinska Inst, Sweden.
    Halfvarson, Jonas
    Örebro Univ, Sweden.
    Myrelid, Pär
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Surgery in Linköping.
    Sachs, Michael C.
    Karolinska Inst, Sweden.
    Nordenvall, Caroline
    Karolinska Univ Hosp, Sweden.
    Söderling, Jonas
    Karolinska Inst, Sweden.
    Ekbom, Anders
    Karolinska Inst, Sweden.
    Neovius, Martin
    Karolinska Inst, Sweden.
    Ludvigsson, Jonas F.
    Karolinska Inst, Sweden; Orebro Univ, Sweden; Univ Nottingham, England; Columbia Univ Coll Phys and Surg, NY USA.
    Askling, Johan
    Karolinska Inst, Sweden.
    Olen, Ola
    Karolinska Inst, Sweden; Sachs Children and Youth Hosp, Sweden.
    Incidence and Treatment of Patients Diagnosed With Inflammatory Bowel Diseases at 60 Years or Older in Sweden2018In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 154, no 3, p. 518-+Article in journal (Refereed)
    Abstract [en]

    BACKGROUND amp; AIMS: Diagnosis of inflammatory bowel diseases (IBD) is increasing among elderly persons (60 years or older). We performed a nationwide population-based study to estimate incidence and treatment of IBD. METHODS: We identified all incident IBD cases in Sweden from 2006 through 2013 using national registers and up to 10 matched population comparator subjects. We collected data on the patients health care contacts and estimated incidence rates, health service burden, pharmacologic treatments, extra-intestinal manifestations, and surgeries in relation to age of IBD onset (pediatric, amp;lt;18 years; adults, 18-59 years; elderly, amp;gt;= 60 years). RESULTS: Of 27,834 persons diagnosed with incident IBD, 6443 (23%) had a first diagnosis of IBD at 60 years or older, corresponding to an incidence rate of 35/100,000 person-years (10/100,000 person-years for Crohns disease, 19/100,000 person-years for ulcerative colitis, and 5/100,000 person-years for IBD unclassified). During a median follow-up period of 4.2 years (range, 0-9 years), elderly patients had less IBD-specific outpatient health care but more IBD-related hospitalizations and overall health care use than adult patients with IBD. Compared with patients with pediatric or adult-onset IBD, elderly patients used fewer biologics and immunomodulators but more systemic corticosteroids. Occurrence of extra-intestinal manifestations was similar in elderly and adult patients, but bowel surgery was more common in the elderly (13% after 5 years vs 10% in adults) (Pamp;lt;.001). The absolute risk of bowel surgery was higher in the elderly than in the general population, but in relative terms, the risk increase was larger in younger age groups. CONCLUSIONS: In a nationwide cohort study in Sweden, we associated diagnosis of IBD at age 60 years or older with a lower use of biologics and immunomodulators but higher absolute risk of bowel surgery, compared with diagnosis at a younger age. The large differences in pharmacologic treatment of adults and elderly patients are not necessarily because of a milder course of disease and warrant further investigation.

  • 9.
    Halfvarson, Jonas
    et al.
    Division of Gastroenterology, Department of Medicine, Örebro University Hospital, Örebro, Sweden.
    Bodin, Lennart
    Clinical Research Center, Örebro University Hospital, Örebro, Sweden.
    Tysk, Curt
    Division of Gastroenterology, Department of Medicine, Örebro University Hospital, Örebro, Sweden.
    Lindberg, Eva
    Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Järnerot, Gunnar
    Division of Gastroenterology, Department of Medicine, Örebro University Hospital, Örebro, Sweden.
    Inflammatory bowel disease in a Swedish twin cohort: a long-term follow-up of concordance and clinical characteristics2003In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 124, no 7, p. 1767-1773Article in journal (Refereed)
    Abstract [en]

    Background & Aims:

    In 1988, we reported the first twin study in inflammatory bowel disease. The aim of the current study was to follow up these twins regarding new cases of inflammatory bowel disease and Crohn’s disease characteristics using the Vienna classification.

    Methods:

    The official Swedish population register and the cause of death register were used to search for the twins. All living patients were interviewed.

    Results:

    Three monozygotic twins earlier classified as healthy had been diagnosed with inflammatory bowel disease (ulcerative colitis, n = 2; Crohn’s disease, n = 1). Retrospectively, all 3 were symptomatic at the original survey. This changed the pair concordance in monozygotic twins from 6.3% to 18.8% in ulcerative colitis and from 44.4% to 50.0% in Crohn’s disease. A high degree of concordance regarding age at diagnosis, disease location at diagnosis and during the course, and disease behavior was found in concordant monozygotic twin pairs with Crohn’s disease. Seven of 9 pairs were identical in 3 or more of these disease characteristics compared with an expected number of 1.5 (P = 0.000076).

    Conclusions:

    This study confirms that the genetic influence is stronger in Crohn’s disease than in ulcerative colitis. A remarkable phenotype similarity within concordant pairs with Crohn’s disease was found using the Vienna classification.

  • 10.
    Järnerot, Gunnar
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Gastroenterology and Hepatology.
    Hertervig, Erik
    Friis-Liby, Ingalill
    Blomquist, Lars
    Karlén, Per
    Grännö, Christer
    Vilien, Mogens
    Ström, Magnus
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Gastroenterology and Hepatology. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Danielsson, Åke
    Verbaan, Hans
    Hellström, Per M
    Magnuson, Anders
    Curman, Bengt
    Infliximab as rescue therapy in severe to moderately severe ulcerative colitis: A randomized, placebo-controlled study2005In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 128, no 7, p. 1805-1811Article in journal (Refereed)
    Abstract [en]

    Background & Aims: Despite treatment with corticosteroids, severe to moderately severe attacks of ulcerative colitis have a high colectomy rate. We intended to find a rescue therapy other than cyclosporin A, which imposes a high risk of side effects and cyclosporine-related mortality. Methods: This was a randomized double-blind trial of infliximab or placebo in severe to moderately severe ulcerative colitis not responding to conventional treatment. Patients were randomized to infliximab/placebo either on day 4 after the initiation of corticosteroid treatment if they fulfilled the index criteria for fulminant ulcerative colitis on day 3 or on day 6-8 if they fulfilled index criteria on day 5-7 for a severe or moderately severe acute attack of ulcerative colitis. Results were analyzed according to the intention-to-treat principle. The primary end point was colectomy or death 3 months after randomization. Secondary end points were clinical and endoscopic remission at that time in patients who did not undergo operation. Results: Forty-five patients were included (24 infliximab and 21 placebo). No patient died. Seven patients in the infliximab group and 14 in the placebo group had a colectomy (P =. 017, odds ratio, 4.9, 95% confidence interval, 1.4-17) within 3 months after randomization. No serious side effects occurred. Three patients in the placebo group required operation for septic complications. Conclusions: Infliximab 4-5 mg/kg is an effective and safe rescue therapy in patients experiencing an acute severe or moderately severe attack of ulcerative colitis not responding to conventional treatment. © 2005 by the American Gastroenterological Association.

  • 11.
    Koch, Stefan
    et al.
    Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia.
    Nava, Porfirio
    Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia.
    Addis, Caroline
    Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia.
    Kim, Wooki
    Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia; Department of Pediatrics, Emory University, Atlanta, Georgia.
    Denning, Timothy L.
    Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia; Department of Pediatrics, Emory University, Atlanta, Georgia.
    Li, Linheng
    Stowers Institute for Medical Research, Kansas City, Missouri.
    Parkos, Charles A.
    Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia.
    Nusrat, Asma
    Epithelial Pathobiology Unit, Department of Pathology and Laboratory Medicine, Emory University, Atlanta, Georgia.
    The Wnt antagonist Dkk1 regulates intestinal epithelial homeostasis and wound repair2011In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 141, no 1, p. 259-268Article in journal (Refereed)
    Abstract [en]

    Background & Aims

    Dkk1 is a secreted antagonist of the Wnt/β-catenin signaling pathway. It is induced by inflammatory cytokines during colitis and exacerbates tissue damage by promoting apoptosis of epithelial cells. However, little is known about the physiologic role of Dkk1 in normal intestinal homeostasis and during wound repair following mucosal injury. We investigated whether inhibition of Dkk1 affects the morphology and function of the adult intestine.

    Methods

    We used doubleridge mice (Dkk1d/d), which have reduced expression of Dkk1, and an inhibitory Dkk1 antibody to modulate Wnt/β-catenin signaling in the intestine. Intestinal inflammation was induced with dextran sulfate sodium (DSS), followed by a recovery period in which mice were given regular drinking water. Animals were killed before, during, or after DSS administration; epithelial homeostasis and the activity of major signaling pathways were investigated by morphometric analysis, bromo-2′-deoxyuridine incorporation, and immunostaining.

    Results

    Reduced expression of Dkk1 increased proliferation of epithelial cells and lengthened crypts in the large intestine, which was associated with increased transcriptional activity of β-catenin. Crypt extension was particularly striking when Dkk1 was inhibited during acute colitis. Dkk1d/dmice recovered significantly faster from intestinal inflammation but exhibited crypt architectural irregularities and epithelial hyperproliferation compared with wild-type mice. Survival signaling pathways were concurrently up-regulated in Dkk1d/d mice, including the AKT/β-catenin, ERK/Elk-1, and c-Jun pathways.

    Conclusions

    Dkk1, an antagonist of Wnt/β-catenin signaling, regulates intestinal epithelial homeostasis under physiologic conditions and during inflammation. Depletion of Dkk1 induces a strong proliferative response that promotes wound repair after colitis.

  • 12.
    Larsson, Marie
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Molecular Virology .
    The dendritic cell: The Immune system's adjuvant-a strategy to develop a HCV vaccine?2006In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 130, no 2, p. 603-606Other (Other academic)
    Abstract [en]

    [No abstract available]

  • 13.
    Larsson, Mats
    et al.
    Linköping University, Center for Medical Image Science and Visualization (CMIV). Linköping University, Department of Clinical and Experimental Medicine, Gastroenterology and Hepatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Endocrinology and Gastroenterology UHL.
    Tillisch, Kirsten
    UCLA, Los Angeles, USA.
    Craig, Bud
    Barrow Neurological Institute, Phoenix, Arizona.
    Engström, Maria
    Linköping University, Center for Medical Image Science and Visualization (CMIV). Linköping University, Department of Medical and Health Sciences, Radiology. Linköping University, Faculty of Health Sciences.
    Labus, Jennifer
    UCLA, Los Angeles, USA.
    Naliboff, Bruce
    UCLA, Los Angeles, USA.
    Lundberg, Peter
    Linköping University, Center for Medical Image Science and Visualization (CMIV). Linköping University, Department of Medical and Health Sciences, Radiation Physics. Linköping University, Department of Medical and Health Sciences, Radiology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Radiation Physics. Östergötlands Läns Landsting, Center for Diagnostics, Department of Radiology in Linköping.
    Ström, Magnus
    Linköping University, Center for Medical Image Science and Visualization (CMIV). Linköping University, Department of Clinical and Experimental Medicine, Gastroenterology and Hepatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Endocrinology and Gastroenterology UHL.
    Mayer, Emeran
    UCLA, Los Angeles, USA.
    Walter, Susanna
    Linköping University, Center for Medical Image Science and Visualization (CMIV). Linköping University, Department of Clinical and Experimental Medicine, Gastroenterology and Hepatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Endocrinology and Gastroenterology UHL.
    Brain Responses to Visceral Stimuli Reflect Visceral Sensitivity Thresholds in Patients With Irritable Bowel Syndrome2012In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 142, no 3, p. 463-472Article in journal (Refereed)
    Abstract [en]

    BACKGROUND & AIMS:

    Only a fraction of patients with irritable bowel syndrome (IBS) have increased perceptual sensitivity to rectal distension, indicating differences in processing and/or modulation of visceral afferent signals. We investigated the brain mechanisms of these perceptual differences.

    METHODS:

    We analyzed data from 44 women with IBS and 20 female healthy subjects (controls). IBS symptom severity was determined by a severity scoring system. Anxiety and depression symptoms were assessed using the hospital anxiety and depression score. Blood oxygen level-dependent signals were measured by functional magnetic resonance imaging during expectation and delivery of high (45 mmHg) and low (15 mmHg) intensity rectal distensions. Perception thresholds to rectal distension were determined in the scanner. Brain imaging data were compared among 18 normosensitive and 15 hypersensitive patients with IBS and 18 controls. Results were reported significant if peak P-values were ≤.05, with family-wise error correction in regions of interest.

    RESULTS:

    The subgroups of patients with IBS were similar in age, symptom duration, psychological symptoms, and IBS symptom severity. Although brain responses to distension were similar between normosensitive patients and controls, hypersensitive patients with IBS had greater activation of insula and reduced deactivation in pregenual anterior cingulate cortex during noxious rectal distensions, compared to controls and normosensitive patients with IBS. During expectation of rectal distension, normosensitive patients with IBS had more activation in right hippocampus than controls.

    CONCLUSIONS:

    Despite similarities in symptoms, hyper- and normosensitive patients with IBS differ in cerebral responses to standardized rectal distensions and their expectation, consistent with differences in ascending visceral afferent input.

  • 14.
    Lesage, S
    et al.
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Chamaillard, M
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Colombel, JF
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Belaiche, J
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Cizard, JP
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Tysk, C
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Almer, Sven
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Gastroenterology and Hepatology . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Gassull, MA
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Binder, V
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Zouali, H
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Thomas, G
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Hugot, JP
    Fdn Jean Dausset, Paris, France Epimad, Lille, France Getaid, Liege, Belgium Ewggp Ibd, Paris, France Irebro Hosp, Irebro, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden Hosp Germans Trias & Pujol, Badalona, Spain Herlev Hosp, DK-2730 Herlev, Denmark.
    Protective effect of CYP2D6*4 allele in ulcerative colitis disease.2000In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 118, no 4, p. 1805-Conference paper (Other academic)
  • 15.
    Lind, Tore
    et al.
    Department of Surgery, Kärnsjukhuset, Skövde, Sweden.
    Mégraud, Francis
    Laboratoire de Bactériologie, Hôpital Pellegrin, Bordeaux, France.
    Unge, Peter
    Department of Internal Medicine, Sandvikens Hospital, Sandviken, Sweden.
    Bayerdörffer, Ekkehard
    Medizinische Klinik I–Gastroenterologie, Universitätsklinikum Carl Gustav Carus, Dresden, Germany.
    O'Morain, Colm
    Department of Gastroenterology, Meath/Adelaide Hospital, Trinity College, Dublin, Ireland.
    Spiller, Robin
    Division of Gastroenterology, Queen's Medical Centre, Nottingham, England.
    Veldhuyzen van Zanten, Sander
    Department of Medicine, Queen Elisabeth II Hospital, Halifax, Nova Scotia, Canada.
    Dev Bardhan, Karna
    Rotherham General Hospitals, Rotherham, England.
    Hellblom, Magnus
    Department of Medicine, Lasarettet, Östersund, Sweden.
    Wrangstadh, Lars
    Astra Hässle, Mölndal, Sweden.
    Zeijlon, Lars
    Astra Hässle, Mölndal, Sweden.
    Cederberg, Christer
    Astra Hässle, Mölndal, Sweden.
    The MACH2 study: Role of omeprazole in eradication of Helicobacter pylori with 1-week triple therapies1999In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 116, no 2, p. 248-253Article in journal (Refereed)
    Abstract [en]

    Background & Aims: The role of omeprazole in triple therapy and the impact of Helicobacter pylori resistance on treatment outcome are not established. This study investigated the role of omeprazole and influence of primary H. pylori resistance on eradication and development of secondary resistance.

    Methods: Patients (n = 539) with a history of duodenal ulcer and a positive H. pylori screening test result were randomized into 4 groups. OAC group received 20 mg omeprazole, 1000 mg amoxicillin, and 500 mg clarithromycin; OMC group received 20 mg omeprazole, 400 mg metronidazole, and 250 mg clarithromycin; and AC (amoxicillin, 1000 mg, and clarithromycin, 500 mg) and MC (metronidazole, 400 mg, and clarithromycin, 250 mg) groups received no omeprazole. All doses were administered twice daily for 1 week. H. pylori status was assessed before and after therapy by 13C-urea breath test. Susceptibility testing was performed at entry and in patients with persistent infection after therapy.

    Results: Eradication (intention to treat [n = 514]/per protocol [n = 449]) was 94%/95% for OAC, 26%/25% for AC (P < 0.001), 87%/91% for OMC, and 69%/72% for MC (P < 0.001). Primary resistance was 27% for metronidazole, 3% for clarithromycin, and 0% for amoxicillin. Eradication in primary metronidazole-susceptible/-resistant strains was 95%/76% for OMC and 86%/43% for MC. Secondary metronidazole and clarithromycin resistance each developed in 12 patients: 8 treated with omeprazole and 16 without omeprazole.

    Conclusions: Addition of omeprazole achieves high eradication rates, reduces the impact of primary resistance, and may decrease the risk of secondary resistance compared with regimens containing only two antibiotics.

  • 16.
    Ludvigsson, Jonas F.
    et al.
    Örebro University Hospital.
    Montgomery, S.M.
    Department of Medicine, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden, Clinical Research Center, Örebro University Hospital, Linkoping, Sweden.
    Ekbom, A.
    Department of Medicine, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden, Harvard Medical School, Boston, MA, United States.
    Celiac disease and risk of adverse fetal outcome: A population-based cohort study2005In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 129, no 2, p. 454-463Article in journal (Refereed)
    Abstract [en]

    Background & Aims: Studies of maternal celiac disease (CD) and fetal outcome are inconsistent, and low statistical power is likely to have contributed to this inconsistency. We investigated the risk of adverse outcomes in women with CD diagnosed prior to pregnancy and in women who did not receive a diagnosis of CD until after the delivery. Methods: A national register-based cohort study restricted to women aged 15-44 years with singleton live born infants was used. We identified 2078 offspring to women who had received a diagnosis of CD (1964-2001): 1149 offspring to women diagnosed prior to birth and 929 offspring to women diagnosed after infant birth. Main outcome measures were: intrauterine growth retardation, low birth weight (

  • 17.
    Mahajan, Vineet
    et al.
    Medical University of Graz.
    Klingstedt, Therése
    Linköping University, Department of Physics, Chemistry and Biology, Biochemistry. Linköping University, The Institute of Technology.
    Simon, Rozalyn
    Linköping University, Department of Physics, Chemistry and Biology, Chemistry. Linköping University, Faculty of Science & Engineering.
    Nilsson, Peter
    Linköping University, Department of Physics, Chemistry and Biology, Organic Chemistry. Linköping University, The Institute of Technology.
    Thueringer, Andrea
    Medical University of Graz.
    Kashofer, Karl
    Medical University of Graz.
    Haybaeck, Johannes
    Medical University of Graz.
    Denk, Helmut
    Medical University of Graz.
    Abuja, Peter M
    Medical University of Graz.
    Zatloukal, Kurt
    Medical University of Graz.
    Cross beta-Sheet Conformation of Keratin 8 Is a Specific Feature of Mallory-Denk Bodies Compared With Other Hepatocyte Inclusions2011In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 141, no 3, p. 1080-U428Article in journal (Refereed)
    Abstract [en]

    BACKGROUND andamp; AIMS: Mallory-Denk bodies (MDBs) are cytoplasmic protein aggregates in hepatocytes in steato-hepatitis and other liver diseases. We investigated the molecular structure of keratin 8 (K8) and 18 (K18), sequestosome 1/p62, and ubiquitin, which are the major constituents of MDBs, to investigate their formation and role in disease pathogenesis. METHODS: Luminescent conjugated oligothiophenes (LCOs), h-HTAA, and p-FTAA are fluorescent amyloid ligands that specifically bind proteins with cross beta-sheet conformation. We used LCOs to investigate conformational changes in MDBs in situ in human and murine livers as well as in transfection studies. RESULTS: LCO analysis showed cross beta-sheet conformation in human MDBs from patients with alcoholic and nonalcoholic steatohepatitis or hepatocellular carcinoma, but not in intracellular hyaline bodies, alpha(1)-antitrypsin deficiency, or ground-glass inclusions. LCOs bound to MDBs induced by 3,5diethoxycarbonyl-1,4-dihydrocollidine feeding of mice at all developmental stages. CHO-K1 cells transfected with various combinations of SQSTM1/p62, ubi, and Krt8/Krt18 showed that K8 was more likely to have cross beta-sheet conformation than K18, whereas p62 never had cross beta-sheet conformation. The different conformational properties of K8 and K18 were also shown by circular dichroism analysis. CONCLUSIONS: K8 can undergo conformational changes from predominantly alpha-helical to cross beta-sheet, which would allow it to form MDBs. These findings might account for the observation that krt8(-/-) mice do not form MDBs, whereas its excess facilitates MDB formation. LCOs might be used in diagnosis of liver disorders; they can be applied to formalin-fixed, paraffin-embedded tissues to characterize protein aggregates in liver cells.

  • 18. Morren, GL
    et al.
    Walter, Susanna
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Gastroenterology and Hepatology . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Hallböök, Olof
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Surgery . Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Surgery in Östergötland.
    Bodemar, Göran
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Gastroenterology and Hepatology . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Medical treatment of patients with faecal incontinence but without diarrhoea.2000In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 118, no 4, p. 5468-Conference paper (Other academic)
  • 19.
    Nasr, Patrik
    et al.
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Gastroentorology.
    Forsgren, Mikael F.
    Linköping University, Department of Medical and Health Sciences, Division of Radiological Sciences. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Radiation Physics. Linköping University, Center for Medical Image Science and Visualization (CMIV). Wolfram MathCore AB, Linköping, Sweden.
    Ignatova, Simone
    Linköping University, Department of Clinical and Experimental Medicine, Divison of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Clinical pathology.
    Dahlström, Nils
    Linköping University, Department of Medical and Health Sciences, Division of Radiological Sciences. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Radiology in Linköping. Linköping University, Center for Medical Image Science and Visualization (CMIV).
    Cedersund, Gunnar
    Linköping University, Department of Biomedical Engineering, Division of Biomedical Engineering. Linköping University, Faculty of Science & Engineering. Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Medicine and Health Sciences.
    Dahlqvist Leinhard, Olof
    Linköping University, Department of Medical and Health Sciences, Division of Radiological Sciences. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Radiation Physics. Linköping University, Center for Medical Image Science and Visualization (CMIV).
    Norén, Bengt
    Linköping University, Department of Medical and Health Sciences, Division of Radiological Sciences. Region Östergötland, Center for Diagnostics, Department of Radiology in Linköping. Linköping University, Center for Medical Image Science and Visualization (CMIV). Linköping University, Faculty of Medicine and Health Sciences.
    Ekstedt, Mattias
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Gastroentorology.
    Lundberg, Peter
    Linköping University, Department of Medical and Health Sciences, Division of Radiological Sciences. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Radiation Physics. Linköping University, Center for Medical Image Science and Visualization (CMIV).
    Kechagias, Stergios
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Gastroentorology.
    Using a 3% Proton Density Fat Fraction as a Cut-off Value Increases Sensitivity of Detection of Hepatic Steatosis, Based on Results from Histopathology Analysis2017In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 153, no 1, p. 53-+Article in journal (Refereed)
    Abstract [en]

    It is possible to estimate hepatic triglyceride content by calculating the proton density fat fraction (PDFF), using proton magnetic resonance spectroscopy (less thansuperscriptgreater than1less than/superscriptgreater thanH-MRS), instead of collecting and analyzing liver biopsies to detect steatosis. However, the current PDFF cut-off value (5%) used to define steatosis by magnetic resonance was derived from studies that did not use histopathology as the reference standard. We performed a prospective study to determine the accuracy of less thansuperscriptgreater than1less than/superscriptgreater thanH-MRS PDFF in measurement of steatosis using histopathology analysis as the standard. We collected clinical, serologic, less thansuperscriptgreater than1less than/superscriptgreater thanH-MRS PDFF, and liver biopsy data from 94 adult patients with increased levels of liver enzymes (6 months or more) referred to the Department of Gastroenterology and Hepatology at Linköping University Hospital in Sweden from 2007 through 2014. Steatosis was graded using the conventional histopathology method and fat content was quantified in biopsy samples using stereological point counts (SPCs). We correlated less thansuperscriptgreater than1less than/superscriptgreater thanH-MRS PDFF findings with SPCs (r = 0.92; P less than.001). less thansuperscriptgreater than1less than/superscriptgreater thanH-MRS PDFF results correlated with histopathology results (ρ = 0.87; P less than.001), and SPCs correlated with histopathology results (ρ = 0.88; P less than.001). All 25 subjects with PDFF values of 5.0% or more had steatosis based on histopathology findings (100% specificity for PDFF). However, of 69 subjects with PDFF values below 5.0% (negative result), 22 were determined to have steatosis based on histopathology findings (53% sensitivity for PDFF). Reducing the PDFF cut-off value to 3.0% identified patients with steatosis with 100% specificity and 79% sensitivity; a PDFF cut-off value of 2.0% identified patients with steatosis with 94% specificity and 87% sensitivity. These findings might be used to improve non-invasive detection of steatosis.

  • 20. Olsson, R
    et al.
    Boberg, KM
    de Muckadell, OS
    Lindgren, S
    Hultcrantz, R
    Folvik, G
    Bell, H
    Gangsoy-Kristiansen, M
    Matre, J
    Rydning, A
    Wikman, O
    Danielsson, A
    Sandberg Gertzén, Hanna
    Örebro University Hospital.
    Ung, KA
    Eriksson, A
    Loof, L
    Prytz, H
    Marschall, HU
    Broome, U
    High-dose ursodeoxycholic acid in primary sclerosing cholangitis: a 5-year multicenter, randomized, controlled study.2005In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 129, no 5, p. 1464-1472Article in journal (Refereed)
    Abstract [en]

    Background & Aims: There is no medical treatment of proven benefit for primary sclerosing cholangitis. This study aimed at studying the effect of a higher dose of ursodeoxycholic acid than previously used on survival, symptoms, biochemistry, and quality of life in this disease. Methods: A randomized placebo-controlled study was performed in tertiary and secondary gastroenterology units. A total of 219 patients were randomized to 17 to 23 mg/kg body weight per day of ursodeoxycholic acid (n = 110) or placebo (n = 109) for 5 years. Follow-up data are available from 97 patients randomized to ursodeoxycholic acid and for 101 randomized to placebo. Quality of life was assessed by using the Medical Outcomes Study 36-item Short-Form Health Survey. Results: The combined end point “death or liver transplantation” occurred in 7 of 97 (7.2%) patients in the ursodeoxycholic acid group vs 11 of 101 (10.9%) patients in the placebo group (P = .368; 95% confidence interval, −12.2% to 4.7%). The occurrence of liver transplantation as a single end point showed a similar positive trend for ursodeoxycholic acid treatment (5/97 [5.2%] vs 8/101 [7.9%]; 95% confidence interval, −10.4% to 4.6%). Three ursodeoxycholic acid and 4 placebo patients died from cholangiocarcinoma, and 1 placebo patient died from liver failure. Alkaline phosphatase and alanine aminotransferase tended to decrease during the first 6 months. There were no differences between the 2 groups in symptoms or quality of life. Analyses of serum ursodeoxycholic acid concentration gave no evidence that noncompliance may have influenced the results. Conclusions: This study found no statistically significant beneficial effect of a higher dose of ursodeoxycholic acid than previously used on survival or prevention of cholangiocarcinoma in primary sclerosing cholangitis.

  • 21. POPE, CE
    et al.
    Ask, Per
    Linköping University, Department of Biomedical Engineering, Physiological Measurements. Linköping University, The Institute of Technology.
    DEBLAN, H
    WINGATE, DL
    MEASUREMENT OF INSTANTANEOUS FLOW VELOCITY IN THE HUMAN GASTROINTESTINAL-TRACT1988In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 95, no 3Article in journal (Refereed)
  • 22.
    Sagar, ME
    et al.
    Karolinska Inst, Stockholm, Sweden Univ Uppsala Hosp, Uppsala, Sweden Linkoping Univ, Linkoping, Sweden.
    Bertilsson, L
    Karolinska Inst, Stockholm, Sweden Univ Uppsala Hosp, Uppsala, Sweden Linkoping Univ, Linkoping, Sweden.
    Stridsberg, M
    Karolinska Inst, Stockholm, Sweden Univ Uppsala Hosp, Uppsala, Sweden Linkoping Univ, Linkoping, Sweden.
    Mard, S
    Kjellin, A
    Karolinska Inst, Stockholm, Sweden Univ Uppsala Hosp, Uppsala, Sweden Linkoping Univ, Linkoping, Sweden.
    Seensalu, R
    Karolinska Inst, Stockholm, Sweden Univ Uppsala Hosp, Uppsala, Sweden Linkoping Univ, Linkoping, Sweden.
    The effects of long-term omeprazole therapy on gastrin, pepsinogen I, and chromogranin A concentrations are related to CYP2C19 polymorphism.2000In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 118, no 4, p. 4890-Conference paper (Other academic)
  • 23.
    Söderholm, Johan D
    et al.
    Linköping University, Department of Biomedicine and Surgery, Surgery. Linköping University, Faculty of Health Sciences.
    Holmgren Peterson, Kajsa
    Linköping University, Department of Molecular and Clinical Medicine, Medical Microbiology. Linköping University, Faculty of Health Sciences.
    Olaison, Gunnar
    Linköping University, Department of Biomedicine and Surgery, Surgery. Linköping University, Faculty of Health Sciences.
    Franzén, Lennart E.
    Department of Pathology, Lund University–MAS, Malmö.
    Weström, Björn
    Department of Animal Physiology, Lund University, Lund, Sweden.
    Magnusson, Karl-Eric
    Linköping University, Department of Molecular and Clinical Medicine, Medical Microbiology. Linköping University, Faculty of Health Sciences.
    Sjödahl, Rune
    Linköping University, Department of Biomedicine and Surgery, Surgery. Linköping University, Faculty of Health Sciences.
    Epithelial permeability to proteins in the noninflamed ileum of Crohn's disease?1999In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 117, no 1, p. 65-72Article in journal (Refereed)
    Abstract [en]

    Background & Aims: Crohn's disease (CD) is associated with a disturbed intestinal barrier. Permeability studies have focused on inert molecules, but little is known about transepithelial transport of macromolecules with antigenic potential in humans. The aim of this study was to quantify permeation and to characterize passage routes for macromolecules in ileal mucosa in CD.

    Methods: Noninflamed and inflamed ileal mucosa specimens from patients with CD (n = 12) and ileal specimens from patients with colon cancer (n = 7) were studied regarding transmucosal permeation of ovalbumin, dextran (mol wt, 40,000), and 51Cr-EDTA for 90 minutes in vitro in Ussing chambers. Transepithelial passage routes for fluorescent ovalbumin and dextran 40,000 were investigated by confocal microscopy.

    Results: Noninflamed ileum from CD patients showed increased permeation of ovalbumin compared with ileum from colon cancer patients (P < 0.05). Dextran permeation was equal in the three groups, whereas 51Cr-EDTA permeability was increased in inflamed ileum. Ovalbumin passed both transcellularly and paracellularly, but dextran followed a strictly paracellular route. Both markers were subsequently endocytosed by cells of the lamina propria.

    Conclusions: Noninflamed ileal mucosa from patients with CD shows increased epithelial permeability to ovalbumin, probably by augmented transcytosis. This increase in antigen load to the lamina propria could be an initiating pathogenic event in CD.

  • 24.
    Söderholm, Johan D
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Surgery . Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Surgery in Östergötland.
    Juliusson, Gunnar
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Oncology . Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Haematology UHL.
    Sjödahl, Rune
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Surgery . Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Surgery in Östergötland.
    Long-term endoscopic remission in a case of Crohn's disease after autologous bone marrow transplantation.2000In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 118, no 4, p. 4212-Conference paper (Other academic)
  • 25.
    Söderholm, Johan D
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Surgery . Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Surgery in Östergötland.
    Wiren, M
    Linkoping Univ, Linkoping, Sweden McMaster Univ, Hamilton, ON, Canada.
    Franzén, Lennart
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Experimental Pathology . Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Pathology and Clinical Genetics.
    Perdue, MH
    Linkoping Univ, Linkoping, Sweden McMaster Univ, Hamilton, ON, Canada.
    Olaison, Gunnar
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Surgery . Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Surgery in Östergötland.
    "Topical" phase effects of acetysalicylic acid on human small bowel epithelium: Inhibition of oxidative phosphorylation and increased tight junction permeability.2000In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 118, no 4, p. 4298-Conference paper (Other academic)
  • 26.
    Söderholm, Johan D
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Surgery. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Surgery in Östergötland.
    Yang, Ping-Chang
    Ceponis, Peter
    Vohra, Angeli
    Riddell, Robert
    Sherman, Philip M
    Perdue, Mary
    Chronic stress induces mast cell-dependent bacterial adherence and initiates mucosal inflammation in rat intestine2002In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 123, p. 1099-1108Article in journal (Refereed)
  • 27. Tibbling, Lita
    et al.
    Ask, Per
    Linköping University, Department of Biomedical Engineering, Physiological Measurements. Linköping University, The Institute of Technology.
    POPE, CE
    ELECTROMYOGRAPHY OF THE HUMAN ESOPHAGUS1982In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 82, no 5Article in journal (Refereed)
  • 28.
    Trulsson, Lena
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Surgery .
    Gasslander, Thomas
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Surgery . Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Surgery in Östergötland.
    Permerth, J
    Svanvik, Joar
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Surgery . Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Surgery in Östergötland.
    The balance of mitogenesis and apoptosis in the rat pancreas in response to CCK-8.2000In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 118, no 4, p. 5324-Conference paper (Other academic)
  • 29.
    Vakil, NB
    et al.
    Univ Wisconsin, Sch Med, Milwaukee, WI 53201 USA Univ Sydney, Nepean Hosp, Dept Med, Penrith, Australia Linkoping Univ Hosp, Dept Biomed & Surg, S-58185 Linkoping, Sweden AstraZeneca R&D Molndal, Molndal, Sweden.
    Talley, NJ
    Univ Wisconsin, Sch Med, Milwaukee, WI 53201 USA Univ Sydney, Nepean Hosp, Dept Med, Penrith, Australia Linkoping Univ Hosp, Dept Biomed & Surg, S-58185 Linkoping, Sweden AstraZeneca R&D Molndal, Molndal, Sweden.
    Bolling-Sternevald, E
    Univ Wisconsin, Sch Med, Milwaukee, WI 53201 USA Univ Sydney, Nepean Hosp, Dept Med, Penrith, Australia Linkoping Univ Hosp, Dept Biomed & Surg, S-58185 Linkoping, Sweden AstraZeneca R&D Molndal, Molndal, Sweden.
    Junghard, O
    Univ Wisconsin, Sch Med, Milwaukee, WI 53201 USA Univ Sydney, Nepean Hosp, Dept Med, Penrith, Australia Linkoping Univ Hosp, Dept Biomed & Surg, S-58185 Linkoping, Sweden AstraZeneca R&D Molndal, Molndal, Sweden.
    Carlsson, R
    Resolution of H-pylori antrum, corpus or pan-gastritis does not induce heartburn in patients with functional dyspepsia2001In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 120, no 5, p. 1238-Conference paper (Other academic)
  • 30.
    Wallon, Conny
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Surgery. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Surgery, Orthopaedics and Cancer Treatment, Department of Surgery in Östergötland.
    Persborn, Mats
    Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
    Jönsson, Maria
    Linköping University, Department of Clinical and Experimental Medicine, Cell Biology. Linköping University, Faculty of Health Sciences.
    Wang, Arthur
    University of Calgary.
    Phan, Van
    University of Calgary.
    Lampinen, Maria
    Uppsala University.
    Vicario, Maria
    CIBERehd.
    Santos, Javier
    CIBERehd.
    Sherman, Philip M
    University of Toronto.
    Carlson, Marie
    Uppsala University.
    Ericson, Ann-Charlott
    Linköping University, Department of Clinical and Experimental Medicine, Cell Biology. Linköping University, Faculty of Health Sciences.
    McKay, Derek M
    University of Calgary.
    Söderholm, Johan D
    Linköping University, Department of Clinical and Experimental Medicine, Surgery. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Surgery, Orthopaedics and Cancer Treatment, Department of Surgery in Östergötland.
    Eosinophils Express Muscarinic Receptors and Corticotropin-Releasing Factor to Disrupt the Mucosal Barrier in Ulcerative Colitis2011In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 140, no 5, p. 1597-1607Article in journal (Refereed)
    Abstract [en]

    BACKGROUND andamp; AIMS: Altered intestinal barrier function has been implicated in the pathophysiology of ulcerative colitis (UC) in genetic, functional, and epidemiological studies. Mast cells and corticotropinreleasing factor (CRF) regulate the mucosal barrier in human colon. Because eosinophils are often increased in colon tissues of patients with UC, we assessed interactions among mast cells, CRF, and eosinophils in the mucosal barrier of these patients. METHODS: Transmucosal fluxes of protein antigens (horseradish peroxidase) and paracellular markers (51Cr-EDTA, fluorescein isothiocyanate-dextran 4000) were studied in noninflamed, colonic mucosal biopsy samples collected from 26 patients with UC and 53 healthy volunteers (controls); samples were mounted in Ussing chambers. We also performed fluorescence and electron microscopy of human tissue samples, assessed isolated eosinophils, and performed mechanistic studies using in vitro cocultured eosinophils (15HL-60), mast cells (HMC-1), and a colonic epithelial cell line (T84). RESULTS: Colon tissues from patients with UC had significant increases in permeability to protein antigens compared with controls. Permeability was blocked by atropine (a muscarinic receptor antagonist), alpha-helical CRF(9-41) (a CRF receptor antagonist), and lodoxamide (a mast-cell stabilizer). Eosinophils were increased in number in UC tissues (compared with controls), expressed the most M2 and M3 muscarinic receptors of any mucosal cell type, and had immunoreactivity to CRF. In coculture studies, carbachol activation of eosinophils caused production of CRF and activation of mast cells, which increased permeability of T84 epithelial cells to macromolecules. CONCLUSIONS: We identified a neuroimmune intercellular circuit (from cholinergic nerves, via eosinophils to mast cells) that mediates colonic mucosal barrier dysfunction in patients with UC. This circuit might exacerbate mucosal inflammation.

  • 31.
    Weismueller, Tobias J.
    et al.
    University of Bonn, Germany; Hannover Medical Sch, Germany.
    Trivedi, Palak J.
    University of Birmingham, England; University Hospital Birmingham Queen Elizabeth, England.
    Bergquist, Annika
    Karolinska University Hospital, Sweden; Karolinska Institute, Sweden.
    Imam, Mohamad
    Mayo Clin, MN USA; University of North Dakota, ND USA.
    Lenzen, Henrike
    Hannover Medical Sch, Germany.
    Ponsioen, Cyriel Y.
    Academic Medical Centre, Netherlands.
    Holm, Kristian
    National Hospital Norway, Norway.
    Gotthardt, Daniel
    University Hospital Heidelberg, Germany.
    Faerkkilae, Martti A.
    University of Helsinki, Finland.
    Marschall, Hanns-Ulrich
    University of Gothenburg, Sweden.
    Thorburn, Douglas
    Royal Free Hospital, England.
    Weersma, Rinse K.
    University of Groningen, Netherlands; University of Medical Centre Groningen, Netherlands.
    Fevery, Johan
    University Hospital Gasthuisberg, Belgium.
    Mueller, Tobias
    Charite, Germany.
    Chazouilleres, Olivier
    Hop St Antoine, France.
    Schulze, Kornelius
    University of Medical Centre Hamburg Eppendorf, Germany.
    Lazaridis, Konstantinos N.
    Mayo Clin, MN USA.
    Almer, Sven
    Linköping University, Department of Clinical and Experimental Medicine, Division of Inflammation Medicine. Linköping University, Faculty of Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Gastroentorology.
    Pereira, Stephen P.
    UCL, England.
    Levy, Cynthia
    University of Miami, FL USA.
    Mason, Andrew
    University of Alberta, Canada.
    Naess, Sigrid
    National Hospital Norway, Norway; National Hospital Norway, Norway; University of Oslo, Norway.
    Bowlus, Christopher L.
    University of Calif Davis, CA 95616 USA.
    Floreani, Annarosa
    University of Padua, Italy.
    Halilbasic, Emina
    Medical University of Vienna, Austria.
    Yimam, Kidist K.
    Calif Pacific Medical Centre, CA USA.
    Milkiewicz, Piotr
    Pomeranian Medical University, Poland; Medical University of Warsaw, Poland.
    Beuers, Ulrich
    Academic Medical Centre, Netherlands.
    Huynh, Dep K.
    Royal Adelaide Hospital, Australia.
    Pares, Albert
    University of Barcelona, Spain.
    Manser, Christine N.
    University Hospital Zurich USZ, Switzerland.
    Dalekos, George N.
    University of Thessaly, Greece.
    Eksteen, Bertus
    University of Calgary, Canada.
    Invernizzi, Pietro
    University of Milano Bicocca, Italy.
    Berg, Christoph P.
    University of Tubingen, Germany.
    Kirchner, Gabi I.
    University Hospital Regensburg, Germany.
    Sarrazin, Christoph
    Johann Wolfgang Goethe University Hospital, Germany.
    Zimmer, Vincent
    Saarland University, Germany.
    Fabris, Luca
    University of Padua, Italy.
    Braun, Felix
    UKSH, Germany.
    Marzioni, Marco
    University of Politecn Marche, Italy.
    Juran, Brian D.
    Mayo Clin, MN USA.
    Said, Karouk
    Karolinska University Hospital, Sweden; Karolinska Institute, Sweden.
    Rupp, Christian
    University Hospital Heidelberg, Germany.
    Jokelainen, Kalle
    University of Helsinki, Finland.
    Benito de Valle, Maria
    University of Gothenburg, Sweden.
    Saffioti, Francesca
    Royal Free Hospital, England; Royal Free Hospital, England.
    Cheung, Angela
    Mayo Clin, MN USA; University of Helsinki, Finland.
    Trauner, Michael
    Medical University of Vienna, Austria.
    Schramm, Christoph
    University of Medical Centre Hamburg Eppendorf, Germany; University of Medical Centre Hamburg Eppendorf, Germany.
    Chapman, Roger W.
    University of Oxford, England; John Radcliffe Hospital, England.
    Karlsen, Tom H.
    National Hospital Norway, Norway; National Hospital Norway, Norway; University of Oslo, Norway.
    Schrumpf, Erik
    National Hospital Norway, Norway; National Hospital Norway, Norway; University of Oslo, Norway.
    Strassburg, Christian P.
    University of Bonn, Germany.
    Manns, Michael P.
    Hannover Medical Sch, Germany.
    Lindor, Keith D.
    Mayo Clin, MN USA; Mayo Clin, AZ USA; Arizona State University, AZ USA.
    Hirschfield, Gideon M.
    University of Birmingham, England.
    Hansen, Bettina E.
    Erasmus University, Netherlands; University of Toronto, Canada; Toronto Gen Hospital, Canada.
    Boberg, Kirsten M.
    National Hospital Norway, Norway; University of Oslo, Norway.
    Patient Age, Sex, and Inflammatory Bowel Disease Phenotype Associate With Course of Primary Sclerosing Cholangitis2017In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 152, no 8, p. 1975-+Article in journal (Refereed)
    Abstract [en]

    BACKGROUND amp; AIMS: Primary sclerosing cholangitis (PSC) is an orphan hepatobiliary disorder associated with inflammatory bowel disease (IBD). We aimed to estimate the risk of disease progression based on distinct clinical phenotypes in a large international cohort of patients with PSC. METHODS: We performed a retrospective outcome analysis of patients diagnosed with PSC from 1980 through 2010 at 37 centers in Europe, North America, and Australia. For each patient, we collected data on sex, clinician-reported age at and date of PSC and IBD diagnoses, phenotypes of IBD and PSC, and date and indication of IBD-related surgeries. The primary and secondary endpoints were liver transplantation or death (LTD) and hepatopancreatobiliary malignancy, respectively. Cox proportional hazards models were applied to determine the effects of individual covariates on rates of clinical events, with time-to-event analysis ascertained through Kaplan-Meier estimates. RESULTS: Of the 7121 patients in the cohort, 2616 met the primary endpoint (median time to event of 14.5 years) and 721 developed hepatopancreatobiliary malignancy. The most common malignancy was cholangiocarcinoma (n = 594); patients of advanced age at diagnosis had an increased incidence compared with younger patients (incidence rate: 1.2 per 100 patient-years for patients younger than 20 years old, 6.0 per 100 patient-years for patients 21-30 years old, 9.0 per 100 patient-years for patients 31-40 years old, 14.0 per 100 patient-years for patients 4150 years old, 15.2 per 100 patient-years for patients 51-60 years old, and 21.0 per 100 patient-years for patients older than 60 years). Of all patients with PSC studied, 65.5% were men, 89.8% had classical or large-duct disease, and 70.0% developed IBD at some point. Assessing the development of IBD as a time-dependent covariate, Crohns disease and no IBD (both vs ulcerative colitis) were associated with a lower risk of LTD (unadjusted hazard ratio [HR], 0.62; P amp;lt;.001 and HR, 0.90; P =.03, respectively) and malignancy (HR, 0.68; P =.008 and HR, 0.77; P =.004, respectively). Small-duct PSC was associated with a lower risk of LTD or malignancy compared with classic PSC (HR, 0.30 and HR, 0.15, respectively; both P amp;lt;.001). Female sex was also associated with a lower risk of LTD or malignancy (HR, 0.88; P =.002 and HR, 0.68; P amp;lt;.001, respectively). In multivariable analyses assessing the primary endpoint, small-duct PSC characterized a low-risk phenotype in both sexes (adjusted HR for men, 0.23; P amp;lt;.001 and adjusted HR for women, 0.48; P =.003). Conversely, patients with ulcerative colitis had an increased risk of liver disease progression compared with patients with Crohns disease (HR, 1.56; P amp;lt;.001) or no IBD (HR, 1.15; P =.002). CONCLUSIONS: In an analysis of data from individual patients with PSC worldwide, we found significant variation in clinical course associated with age at diagnosis, sex, and ductal and IBD subtypes. The survival estimates provided might be used to estimate risk levels for patients with PSC and select patients for clinical trials.

  • 32.
    Yang, P.
    et al.
    Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ont., Canada.
    Xing, Z.
    Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ont., Canada.
    Berin, C.M.
    Department of Medicine, Division of Clinical Immunology, Mount Sinai School of Medicine, New York, NY, United States.
    Söderholm, Johan D
    Linköping University, Department of Clinical and Experimental Medicine, Surgery . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Anaesthesiology and Surgical Centre, Department of Surgery UHL.
    Feng, B.
    Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ont., Canada.
    Wu, L.
    Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ont., Canada.
    Yeh, C.
    Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ont., Canada.
    TIM-4 Expressed by Mucosal Dendritic Cells Plays a Critical Role in Food Antigen-Specific Th2 Differentiation and Intestinal Allergy2007In: Gastroenterology, ISSN 0016-5085, E-ISSN 1528-0012, Vol. 133, no 5, p. 1522-1533Article in journal (Refereed)
    Abstract [en]

    Background & Aims: Food allergy accounts for significant morbidity. The etiology and immune mechanisms of food allergy, however, have remained poorly understood. In this study, we aimed to determine the role of T-cell immunoglobulin-domain and mucin-domain (TIM)-4, a recently identified member of cell surface molecules, in the pathogenesis of intestinal allergy in a murine model. Methods: We report that TIM-4 as well as costimulatory molecules were up-regulated in intestinal mucosal dendritic cells by in vitro or in vivo exposure to Staphylococcus enterotoxin B (SEB). SEB-conditioned intestinal dendritic cells loaded with a food macromolecule ovalbumin (OVA) induced potent OVA-specific T-helper (Th)2 lymphocyte responses in vitro and such Th2 responses were inhibited completely by TIM-4 blockade. Results: In vivo exposure to both SEB and OVA resulted in OVA-specific Th2 differentiation and intestinal allergic responses including increased serum immunoglobulin E and Th2 cytokine levels, activation of OVA-specific Th2 cells detected both ex vivo and in situ, and mast cell degranulation. Of importance, in vivo abrogation of TIM-4 or its cognate ligand TIM-1 by using a polyclonal antibody remarkably dampened Th2 differentiation and intestinal allergy. Conclusions: Our study thus identifies TIM-4 as a novel molecule critically required for the development of intestinal allergy. © 2007 AGA Institute.

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