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  • 1.
    Abrahamsson, Thomas
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Sherman, Philip M.
    University of Toronto, Canada .
    Editorial Material: Multifaceted Effects of Human Milk Oligosaccharides2014Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 209, nr 3, s. 323-324Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    n/a

  • 2.
    Benson, Mikael
    et al.
    East Hospital, Göteborg, Sweden.
    Jodal, Ulf
    Göteborg University, Sweden.
    Agace, William
    Lund University, Sweden.
    Hellström, Mikael
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Mårild, Staffan
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Rosberg, Sten
    Göteborg University, Sweden.
    Sjöström, Michael
    Umeå University, Sweden.
    Wettergren, Björn
    Jönsson, Susanne
    Svanborg, Catharina
    Lund University, Sweden.
    Interleukin (IL)-6 and IL-8 in children with febrile urinary tract infection and asymptomatic bacteriuria1996Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 174, nr 5, s. 1080-1084Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Urine and serum interleukin (IL)-6 and IL-8 responses were higher in children with febrile urinary tract infection (n = 61) than in those with asymptomatic bacteriuria (n = 39). By univariate analysis, cytokine levels were related to age, sex, reflux, renal scarring, urine leukocytes, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and bacterial properties (P fimbriae but not hemolysin). Multivariate modeling showed that urine IL-6 responses were higher in girls than boys, increased with age, and were positively associated with CRP, ESR, serum IL-6, and urine leukocyte counts. The urine IL-8 response was not influenced by age, but it was influenced by P fimbriae and was associated with ESR, CRP, urine leukocytes, and female sex. The results show that cytokine responses to urinary tract infection vary with the severity of infection and that cytokine activation is influenced by a variety of host and bacterial variables.

  • 3.
    Cardell, Kristina
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Infektionsmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Medicincentrum, Infektionskliniken i Östergötland.
    Åkerlind, Britt
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Klinisk mikrobiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk mikrobiologi.
    Sällberg, Matti
    Division of Clinical Virology, Karolinska Institute at Karolinska University Hospital, Huddinge, Sweden.
    Frydén, Aril
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Infektionsmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Närsjukvården i centrala Östergötland, Infektionskliniken US.
    Excellent response rate to a double dose of the combined hepatitis A and B vaccine in previous nonresponders to hepatitis B vaccine2008Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 198, nr 3, s. 299-304Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Hepatitis B vaccine has been shown to be highly efficient in preventing hepatitis B. However, 5%-10% of individuals fail to develop protective levels (>or=10 mIU/mL) of antibodies to hepatitis B surface antigen (anti-HBs) and are considered to be nonresponders.

    METHODS: A total of 48 nonresponders and 20 subjects naive to the HBV vaccine received a double dose of combined hepatitis A and B vaccine (Twinrix) at 0, 1, and 6 months. The levels of anti-HBs and antibodies to hepatitis A virus (anti-HAV) were determined before vaccination and 1 month after each dose.

    RESULTS: Among 44 nonresponders, protective anti-HBs levels were found in 26 (59%) after the first dose and in 42 (95%) after the third dose. Among the control subjects, the corresponding figures were 10% and 100%, respectively. All subjects seroconverted to anti-HAV. The titers of both anti-HBs and anti-HAV were lower in the previously nonresponsive subjects (P< .01).

    CONCLUSION: Revaccination of nonresponders to the standard hepatitis B vaccine regimen with a double dose of the combined hepatitis A and B vaccine was highly effective. This is most likely explained by the increased dose, a positive bystander effect conferred by the hepatitis A vaccine, or both.

  • 4.
    Connolly-Andersen, Anne-Marie
    et al.
    Umeå University, Sweden.
    Sundberg, Erik
    Umeå University, Sweden.
    Ahlm, Clas
    Umeå University, Sweden.
    Hultdin, Johan
    Umeå University, Sweden.
    Baudin, Maria
    Umeå University, Sweden.
    Larsson, Johanna
    Umeå University, Sweden.
    Dunne, Eimear
    Royal Coll Surgeons Ireland, Ireland.
    Kenny, Dermot
    Royal Coll Surgeons Ireland, Ireland.
    Lindahl, Tomas
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk kemi.
    Ramström, Sofia
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten.
    Nilsson, Sofie
    Umeå University, Sweden.
    Increased Thrombopoiesis and Platelet Activation in Hantavirus-Infected Patients2015Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 212, nr 7, s. 1061-1069Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background. Thrombocytopenia is a common finding during viral hemorrhagic fever, which includes hemorrhagic fever with renal syndrome (HFRS). The 2 main causes for thrombocytopenia are impaired thrombopoiesis and/or increased peripheral destruction of platelets. In addition, there is an increased intravascular coagulation risk during HFRS, which could be due to platelet activation. Methods. Thrombopoiesis was determined by quantification of platelet counts, thrombopoietin, immature platelet fraction, and mean platelet volume during HFRS. The in vivo platelet activation was determined by quantification of soluble P-selectin (sP-selectin) and glycoprotein VI (sGPVI). The function of circulating platelets was determined by ex vivo stimulation followed by flow cytometry analysis of platelet surface-bound fibrinogen and P-selectin exposure. Intravascular coagulation during disease was determined by scoring for disseminated intravascular coagulation (DIC) and recording thromboembolic complications. Results. The levels of thrombopoietin, immature platelet fraction, and mean platelet volume all indicate increased thrombopoiesis during HFRS. Circulating platelets had reduced ex vivo function during disease compared to follow-up. Most interestingly, we observed significantly increased in vivo platelet activation in HFRS patients with intravascular coagulation (DIC and thromboembolic complications) as shown by sP-selectin and sGPVI levels. Conclusions. HFRS patients have increased thrombopoiesis and platelet activation, which contributes to intravascular coagulation.

  • 5.
    Elkington, Paul
    et al.
    Univ Southampton, England.
    Lerm, Maria
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi, infektion och inflammation. Linköpings universitet, Medicinska fakulteten.
    Kapoor, Nidhi
    Florida Hosp Adventist Hlth Syst, FL USA.
    Mahon, Robert
    NIAID, MD 20892 USA.
    Pienaar, Elsje
    Purdue Univ, IN 47907 USA.
    Huh, Dongeun
    Univ Penn, PA 19104 USA.
    Kaushal, Deepak
    Texas Biomed Res Inst, TX USA.
    Schlesinger, Larry S.
    Texas Biomed Res Inst, TX USA.
    In Vitro Granuloma Models of Tuberculosis: Potential and Challenges2019Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 219, nr 12, s. 1858-1866Artikkel, forskningsoversikt (Fagfellevurdert)
    Abstract [en]

    Despite intensive research efforts, several fundamental disease processes for tuberculosis (TB) remain poorly understood. A central enigma is that host immunity is necessary to control disease yet promotes transmission by causing lung immunopathology. Our inability to distinguish these processes makes it challenging to design rational novel interventions. Elucidating basic immune mechanisms likely requires both in vivo and in vitro analyses, since Mycobacterium tuberculosis is a highly specialized human pathogen. The classic immune response is the TB granuloma organized in three dimensions within extracellular matrix. Several groups are developing cell culture granuloma models. In January 2018, NIAID convened a workshop, entitled "3-D Human in vitro TB Granuloma Model" to advance the field. Here, we summarize the arguments for developing advanced TB cell culture models and critically review those currently available. We discuss how integrating complementary approaches, specifically organoids and mathematical modeling, can maximize progress, and conclude by discussing future challenges and opportunities.

  • 6.
    Günaydın, Gökçe
    et al.
    Division of Clinical Immunology, Karolinska Institutet at Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Nordgren, Johan
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin.
    Svensson, Lennart
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin.
    Hammarström, Lennart
    Division of Clinical Immunology, Karolinska Institutet at Karolinska University Hospital Huddinge, Stockholm, Sweden.
    TLR3-dependent antibody response against rotavirus in individuals with immunoglobulin A deficiency2013Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613Artikkel i tidsskrift (Fagfellevurdert)
  • 7.
    Kindberg, Elin
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Molekylär virologi. Linköpings universitet, Hälsouniversitetet.
    Mickiene, Aukse
    Department of Medicine Karolinska University Hospital Huddinge.
    Ax, Cecilia
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Åkerlind, Britt
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Klinisk mikrobiologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk mikrobiologi.
    Vene, Sirkka
    5Swedish Institute for Infectious Disease Control Karolinska Institutet, Stockholm.
    Lindquist, Lars
    Department of Medicine Karolinska University Hospital Huddinge.
    Lundkvist, Åke
    Swedish Institute for Infectious Disease Control Karolinska Institutet, Stockholm.
    Svensson, Lennart
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Molekylär virologi. Linköpings universitet, Hälsouniversitetet.
    A deletion in the chemokine receptor 5 (CCR5) gene is associated with tickborne encephalitis2008Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 197, nr 2, s. 266-269Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Tickborne encephalitis (TBE) virus infections can be asymptomatic or cause moderate to severe injuries of the central nervous system. Why some individuals develop severe disease is unknown, but a role for host genetic factors has been suggested. To investigate whether chemokine receptor CCR5 is associated with TBE, CCR5Δ32 genotyping was performed among Lithuanian patients with TBE (n = 129) or with aseptic meningoencephalitis (n = 76) as well as among control subjects (n = 134). We found individuals homozygous for CCR5Δ32 (P = .026) only among patients with TBE and a higher allele prevalence among patients with TBE compared with the other groups studied. CCR5Δ32 allele prevalence also increased with the clinical severity of disease. © 2007 by the Infectious Diseases Society of America. All rights reserved.

  • 8.
    Kwiecinski, J
    et al.
    Sahlgrenska Academy.
    Josefsson, E
    Sahlgrenska Academy.
    Mitchell, J
    Trinity College, Dublin.
    Higgins, J
    Trinity College, Dublin.
    Magnusson, Mattias
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Reumatologi. Linköpings universitet, Hälsouniversitetet.
    Foster, T
    Trinity College, Dublin.
    Jin, T
    Sahlgrenska Academy.
    Bokarewa, M
    Sahlgrenska Academy.
    Activation of Plasminogen by Staphylokinase Reduces the Severity of Staphylococcus aureusSystemic Systemic Infection2010Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 202, nr 7, s. 1041-1049Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

     

    Background. Theoretical and experimental data support the geographic differentiation strategy as a valuable tool for detecting loci under selection. In the context of Plasmodium falciparum malaria, few populations have been studied, with limited genomic coverage.

    Methods. Wild-type S. aureus strain LS-1, which lacks the ability to produce SAK, was modified by an insertion of the sak gene into its chromosome. The sak gene was integrated in 2 forms—(1) linked to its own promoter and (2) fused to the promoter of the protein A gene—which resulted in the overexpression of SAK. SAK is highly specific for human plg and exhibits almost no activity toward murine plg. To investigate the role played by SAK in a murine infection model, human plg transgenic mice and their wild-type counterparts were inoculated intravenously with congenic S. aureus strains differing in SAK production.

    Results. Human plg transgenic mice inoculated with SAK-expressing strains displayed significantly reduced mortality, less weight loss, and lower bacterial loads in kidneys than did the wild-type mice. No difference in the severity of sepsis was observed between transgenic and wild-type mice infected with a SAK-deficient strain.

    Conclusions. The results suggest that expression of SAK followed by activation of plg alleviates the course of S. aureus sepsis. 

     

     

     

     

     

     

     

     

     

      

     

     

     

     

     

     

     

     

     

     

     

     

     

    Background.

     

    Staphylokinase (SAK) is produced by the majority of Staphylococcus aureus strains. It is an extracellular protein that activates the conversion of human plasminogen (plg) to plasmin. The role played by SAK in staphylococcal infection is unclear.Methods. Wild-type S. aureus strain LS-1, which lacks the ability to produce SAK, was modified by an insertion of the sak gene into its chromosome. The sak gene was integrated in 2 forms—(1) linked to its own promoter and (2) fused to the promoter of the protein A gene—which resulted in the overexpression of SAK. SAK is highly specific for human plg and exhibits almost no activity toward murine plg. To investigate the role played by SAK in a murine infection model, human plg transgenic mice and their wild-type counterparts were inoculated intravenously with congenic S. aureus strains differing in SAK production.Results. Human plg transgenic mice inoculated with SAK-expressing strains displayed significantly reduced mortality, less weight loss, and lower bacterial loads in kidneys than did the wild-type mice. No difference in the severity of sepsis was observed between transgenic and wild-type mice infected with a SAK-deficient strain.Conclusions. The results suggest that expression of SAK followed by activation of plg alleviates the course of S. aureus

    sepsis.

  • 9.
    Modin Larsson, Malin
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Molekylär virologi. Linköpings universitet, Hälsouniversitetet.
    Rydell, Gustaf
    Department of Clinical Chemistry and Transfusion Medicine, Sahlgrenska University Hospital, Göteborg.
    Grahn, Ammi
    Department of Clinical Chemistry and Transfusion Medicine, Sahlgrenska University Hospital, Göteborg.
    Rodríguez-Díaz, Jesús
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Molekylär virologi. Linköpings universitet, Hälsouniversitetet.
    Åkerlind, Britt
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Klinisk mikrobiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Diagnostikcentrum, Klinisk mikrobiologi.
    Hutson, Anne
    Departments of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA .
    Estes, Mary
    Departments of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA.
    Larson, Göran
    Department of Clinical Chemistry and Transfusion Medicine, Sahlgrenska University Hospital, Göteborg.
    Svensson, Lennart
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Molekylär virologi. Linköpings universitet, Hälsouniversitetet.
    Antibody Prevalence and Titer to Norovirus (Genogroup II) Correlate with Secretor (FUT2) but Not with ABO Phenotype or Lewis (FUT3) Genotype2006Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 194, nr 10, s. 1422-1427Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND:

    Histo-blood group antigens and secretor status have been associated with susceptibility to Norovirus infections, which suggests that antibody prevalence and titer might correlate with these phenotypes.

    METHODS:

    Plasma samples (n = 105) from Swedish blood donors that had been genotyped for secretor (FUT2) and Lewis (Le; FUT3) genotypes and phenotyped for ABO and Le blood groups were analyzed for immunoglobulin G antibody prevalence and titers to norovirus genogroup (GG) II.4.

    RESULTS:

    The results showed that nonsecretors (se4128se428) and Lea+b- individuals not only had significantly lower antibody titers than did secretors (P < .0001) and Lea-b+ individuals (P < .0002) but were also significantly more often antibody negative (P < .05). Antibody titers in secretors were not significantly different between individuals of different Le (FUT3) genotypes or different ABO phenotypes.

    CONCLUSIONS:

    Nonsecretors and Lea+b- individuals are significantly less prone to be infected with GGII noroviruses. This new information extends previous knowledge and supports the hypothesis that nonsecretors are relatively but not absolutely resistant to norovirus infections.

  • 10.
    Nayeri, Fariba
    et al.
    Linköpings universitet, Institutionen för molekylär och klinisk medicin, Infektionsmedicin. Linköpings universitet, Hälsouniversitetet.
    Nilsson, Ingela
    Department of Clinical Chemistry, County Hospital, Kalmar.
    Hagberg, Lars
    Department of Infectious Diseases, Sahlgrenska Hospital, Göteborg.
    Brudin, Lars
    Department of Clinical Physiology, County Hospital, Kalmar.
    Roberg, Magnus
    Department of Infectious Diseases, County Hospital, Norrköping, Sweden .
    Söderström, Claes
    Department of Infectious Diseases, County Hospital, Kalmar.
    Forsberg, Pia
    Linköpings universitet, Institutionen för molekylär och klinisk medicin, Infektionsmedicin. Linköpings universitet, Hälsouniversitetet.
    Hepatocyte Growth Factor Levels in Cerebrospinal Fluid: A Comparison between Acute Bacterial and Nonbacterial Meningitis2000Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 181, nr 6, s. 2092-2094Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The organotrophic functions of the hepatocyte growth factor (HGF) have been the subject of several studies. In the more recent studies, this function has been reported in the brain. In the present study, we have measured the levels of HGF in cerebrospinal fluid (CSF) and sera from 78 patients divided into 6 different groups according to central nervous system (CNS) infection and control. Quantitative measurements of HGF in the CSF and serum were performed by an enzyme-linked immunosorbent assay. Elevated values of CSF HGF were found in the patients with acute bacterial/probable bacterial meningitis (P < .001), compared with nonbacterial CNS infections and facial palsy, as well as with a control group without signs of CNS involvement. The values of CSF HGF were not correlated to blood-brain-barrier disruption in the groups. These observations might indicate an intrathecal production of HGF in acute bacterial/probable bacterial meningitis.

  • 11. Pant, Neha
    et al.
    Hultberg, Anna
    Zhao, Yaofeng
    Svensson, Lennart
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Molekylär virologi.
    Pan-Hammarström, Qiang
    Johansen, Kari
    Pouwels, Peter H
    Ruggeri, Franco M
    Hermans, Pim
    Frenken, Leon
    Borén, Thomas
    Marcotte, Harold
    Hammarström, Lennart
    Lactobacilli expressing variable domain of llama heavy-chain antibody fragments (lactobodies) confer protection against rotavirus-induced diarrhea2006Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 194, nr 11, s. 1580-1588Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background. Rotavirus-induced diarrhea poses a worldwide medical problem in causing substantial morbidity and mortality among children in developing countries. We therefore developed a system for passive immunotherapy in which recombinant lactobacilli constitutively express neutralizing variable domain of llama heavy-chain (VHH) antibody fragments against rotavirus. Methods. VHH were expressed in Lactobacillus paracasei, in both secreted and cell surface-anchored forms. Electron microscopy was used to investigate the binding efficacy of VHH-expressing lactobacilli. To investigate the in vivo function of VHH-expressing lactobacilli, a mouse pup model of rotavirus infection was used. Results. Efficient binding of the VHH antibody fragments to rotavirus was shown by enzyme-linked immunosorbent assay and scanning electron microscopy. VHH fragments expressed by lactobacilli conferred a significant reduction in infection in cell cultures. When administered orally, lactobacilli-producing surface-expressed VHH markedly shortened disease duration, severity, and viral load in a mouse model of rotavirus-induced diarrhea when administered both fresh and in a freeze-dried form. Conclusions. Transformed lactobacilli may form the basis of a novel form of prophylactic treatment against rotavirus infections and other diarrheal diseases. © 2006 by the Infectious Diseases Society of America. All rights reserved.

  • 12.
    Rytkönen, Anne
    et al.
    KI.
    Albinger, Barbara
    Hansson-Palo, Paola
    Källström, Helena
    Olcén, Per
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Klinisk mikrobiologi.
    Fredlund, Hans
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Klinisk mikrobiologi.
    Jonsson, Ann-Beth
    Neisseria meningitidis undergoes PilC phase variation and PilC sequence variation during invasive disease.2004Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 189, s. 402-409Artikkel i tidsskrift (Fagfellevurdert)
  • 13.
    Sievers, M.
    et al.
    Medizinische Universitätsklinik, Freiburg, Germany.
    Walker, U. A.
    Medizinische Universitätsklinik, Freiburg, Germany; .
    Sevastianova, K.
    Helsinki University Central Hospital, Finland.
    Setzer, B.
    Medizinische Universitätsklinik, Freiburg, Germany.
    Wågsäter, Dick
    Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden .
    Eriksson, P.
    Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden .
    Yki-Järvinen, H.
    Helsinki University Central Hospital, Finland.
    Sutinen, J.
    Helsinki University Central Hospital, Finland.
    Gene Expression and Immunohistochemistry in Adipose Tissue of HIV Type 1-Infected Patients with Nucleoside Analogue Reverse-Transcriptase Inhibitor-Associated Lipoatrophy2009Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 200, nr 2, s. 252-262Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND:

    Long-term use of both zidovudine (AZT) and stavudine (d4T) is associated with lipoatrophy, but it occurs possibly through different mechanisms.

    METHODS:

    Surgical biopsy specimens of subcutaneous adipose tissue were obtained from 18 human immunodeficiency virus type 1 (HIV-1)-infected lipoatrophic patients (the LA+ group) who were treated with either zidovudine (the AZT+LA+ group; n = 10) or stavudine (the d4T+LA+ group; n = 8) and from 10 nonlipoatrophic HIV-1-infected patients (the LA- group) who received antiretroviral therapy. Mitochondrial DNA (mtDNA) copy numbers, gene expression, and immunohistochemistry data were analyzed.

    RESULTS:

    mtDNA copy numbers were significantly reduced in the LA+ group, compared with the LA- group, and in the d4T+LA+ group, compared with the AZT+LA+ group. The ratio of mtDNA-encoded cytochrome COX3 to nuclear DNA-encoded COX4 expression was significantly lower in the LA+ group than in the LA- group. Compared with the LA- group, the LA+ group had significantly lower expression of genes involved in adipogenesis (SREBP1c and CEBPB), lipid (fatty acid synthase), and glucose (GLUT4) metabolism. Expression of genes involved in mitochondrial biogenesis (PGC1B), apoptosis (FAS), inflammation (IL1B), oxidative stress (PCNA and SOD1), and lamin B was significantly higher in the LA+ group than in the LA- group. The d4T+LA+ group had significantly lower expression of genes involved in mitochondrial biogenesis (POLG1), energy metabolism (the COX3/COX4 ratio), adipogenesis (SREBP1c and CEBPA), perilipin, and hexokinase than did the AZT+LA+ group. There were 7-fold more macrophages in adipose tissue specimens obtained from patients in the LA+ group, compared with the LA- group.

    CONCLUSIONS:

    Lipoatrophy is characterized by mtDNA depletion, inflammation, and signs of apoptosis. Changes were more profound in the d4T+LA+ group than in the AZT+LA+ group

  • 14.
    Telang, S
    et al.
    Univ Louisville, James Graham Brown Canc Ctr, Louisville, KY 40202 USA Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA Univ Illinois, Dept Pathobiol, Urbana, IL 61801 USA Calif State Univ Chico, Dept Biol, Chico, CA USA Linkoping Univ, Fac Hlth Sci, Div Pathol 2, Linkoping, Sweden.
    Vimr, E
    Univ Louisville, James Graham Brown Canc Ctr, Louisville, KY 40202 USA Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA Univ Illinois, Dept Pathobiol, Urbana, IL 61801 USA Calif State Univ Chico, Dept Biol, Chico, CA USA Linkoping Univ, Fac Hlth Sci, Div Pathol 2, Linkoping, Sweden.
    Mahoney, JR
    Univ Louisville, James Graham Brown Canc Ctr, Louisville, KY 40202 USA Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA Univ Illinois, Dept Pathobiol, Urbana, IL 61801 USA Calif State Univ Chico, Dept Biol, Chico, CA USA Linkoping Univ, Fac Hlth Sci, Div Pathol 2, Linkoping, Sweden.
    Law, I
    Univ Louisville, James Graham Brown Canc Ctr, Louisville, KY 40202 USA Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA Univ Illinois, Dept Pathobiol, Urbana, IL 61801 USA Calif State Univ Chico, Dept Biol, Chico, CA USA Linkoping Univ, Fac Hlth Sci, Div Pathol 2, Linkoping, Sweden.
    Lundqvist-Gustafsson, H
    Univ Louisville, James Graham Brown Canc Ctr, Louisville, KY 40202 USA Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA Univ Illinois, Dept Pathobiol, Urbana, IL 61801 USA Calif State Univ Chico, Dept Biol, Chico, CA USA Linkoping Univ, Fac Hlth Sci, Div Pathol 2, Linkoping, Sweden.
    Qian, MW
    Univ Louisville, James Graham Brown Canc Ctr, Louisville, KY 40202 USA Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA Univ Illinois, Dept Pathobiol, Urbana, IL 61801 USA Calif State Univ Chico, Dept Biol, Chico, CA USA Linkoping Univ, Fac Hlth Sci, Div Pathol 2, Linkoping, Sweden.
    Eaton, John Wallace
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Experimentell patologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk patologi och klinisk genetik.
    Strain-specific iron-dependent virulence in Escherichia coli2001Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 184, nr 2, s. 159-165Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    For reasons unknown, certain Escherichia coli strains become highly virulent when injected with hemoglobin or other soluble iron sources. Two clinical isolates (virulent and nonvirulent) showed equivalent hemoglobin-mediated growth acceleration in vitro. However, when injected intraperitoneally into mice without hemoglobin, the virulent strain was cleared more slowly (t(1/2), >4 h vs. <30 min). The virulent E. coli strain had a polysialic acid-containing capsule, whereas the nonvirulent strain did not. Virulent E. coli grown at 20C (which blocks polysialylation) were cleared as rapidly as nonvirulent organisms. In another virulent E. coli strain having abundant outer membrane polysialic acid, targeted deletion of the polysialyltransferase accelerated host clearance and blocked iron-dependent virulence. The iron-dependent virulence of certain E. coli strains may represent the combined effect of slow in vivo clearance-associated, in this case, with outer membrane polysialylation coupled with accelerated growth permitted by iron compounds.

  • 15.
    Widhe, Mona
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Klinisk immunologi. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Infektionsmedicin. Linköpings universitet, Hälsouniversitetet.
    Jarefors, Sara
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Klinisk immunologi. Linköpings universitet, Institutionen för molekylär och klinisk medicin, Infektionsmedicin. Linköpings universitet, Hälsouniversitetet.
    Ekerfelt, Christina
    Linköpings universitet, Institutionen för molekylär och klinisk medicin, Klinisk immunologi. Linköpings universitet, Hälsouniversitetet.
    Vrethem, Magnus
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Neurologi. Linköpings universitet, Institutionen för nervsystem och rörelseorgan, Neurofysiologi. Linköpings universitet, Hälsouniversitetet.
    Bergström, Sven
    Department of Molecular Biology, University of Umeå, Umeå, Sweden.
    Forsberg, Pia
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Infektionsmedicin. Linköpings universitet, Hälsouniversitetet.
    Ernerudh, Jan
    Linköpings universitet, Hälsouniversitetet.
    Borrelia-specific interferon-γ and interleukin-4 secretion in cerebrospinal fluid and blood during Lyme borreliosis in humans: association with clinical outcome2004Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 189, nr 10, s. 1881-1891Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The Borrelia-specific interferon (IFN)-γ and interleukin (IL)-4 responses of 113 patients and control subjects were analyzed using the sensitive enzyme-linked immunospot method. Cerebrospinal fluid (CSF) and blood samples were obtained, during the course of disease, from patients with chronic or nonchronic neuroborreliosis (NB) and from control subjects without NB. Blood samples were obtained from patients with Lyme skin manifestations and from healthy blood donors. Early increased secretion of Borrelia-specific IFN-γ (P < .05) and subsequent up-regulation of IL-4 ( P < .05) were detected in the CSF cells of patients with nonchronic NB. In contrast, persistent Borrelia-specific IFN-γ responses were observed in the CSF cells of patients with chronic NB ( P < .05). In patients with erythema migrans, increased IFN-γ (P < .001 ) was observed in blood samples obtained early during the course of disease, whereas increased IL-4 ( P < .05) was observed after clearance. On the contrary, patients with acrodermatitis chronica atrophicans had Borrelia-specific IFN-γ (P < .001 ), but not IL-4, detected in blood samples. The present data suggest that an initial IFN-γ response, followed by up-regulation of IL-4, is associated with nonchronic manifestations, whereas a persistent IFN-γ response may lead to chronic Lyme borreliosis.

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