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  • 1.
    Casado Bedmar, Maria Teresa
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Heil, Stéphanie
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    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.
    Söderholm, Johan D
    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.
    Keita, Åsa
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Upregulation of intestinal mucosal mast cells expressing VPAC1 in close proximity to vasoactive intestinal polypeptide in inflammatory bowel disease and murine colitis2019In: Neurogastroenterology and Motility, ISSN 1350-1925, E-ISSN 1365-2982, Vol. 31, no 3, article id e13503Article in journal (Refereed)
    Abstract [en]

    Background

    Mast cells (MCs) and vasoactive intestinal polypeptide (VIP) have been proposed as regulators of the intestinal barrier and inflammation. Our aim was to map the distribution in inflammatory bowel disease (IBD) and murine colitis.

    Methods

    MCs, VIP, and VIP‐receptors (VPACs) were quantified by immunofluorescence and enzyme‐immunoassay (EIA) in ileal tissues (villus epithelium (VE) and adjacent VE, ie, VE next to the follicle‐associated epithelium, (FAE)) from Crohn's disease (CD; n = 16) and non‐IBD patients, and in colonic specimens of ulcerative colitis (UC; n = 12) and healthy controls (HCs). In addition, VIP levels were measured in plasma from HCs, non‐IBD, and IBD in remission (CD n = 30; UC n = 30). Colon, ileum, and plasma from mice with dextran sulfate sodium (DSS)‐induced colitis and control mice were analyzed likewise.

    Key Results

    FAE‐adjacent VE in ileum of CD possessed more MCs (P < 0.05) and MCs expressing VPAC1 (P < 0.05), but not VPAC2, compared to controls. Both adjacent and regular VE of CD had more MCs co‐localizing/in close proximity to VIP (P < 0.05). In UC colon, more MCs (P < 0.0005), MCs close to VIP (P < 0.0005), and MCs expressing VPAC1 (P < 0.05) were found compared to controls. VIP levels were elevated in plasma from CD and UC compared to controls (P < 0.0005). Colon of DSS mice showed more MCs and MCs close to VIP (P < 0.05) compared to control mice. In vitro experiments revealed MCs expressing VPACs and internalized VIP after 120 minutes of VIP‐stimulation.

    Conclusions and Inferences

    Communication between MCs and VIP is upregulated during IBD and mice colitis. In CD patients, the epithelium next to FAE seems to be more involved than the surrounding VE, suggesting increased MC‐VIP‐interactions in this intestinal region.

  • 2. da Silva, Stéphanie
    Conséquences d’un stress chronique sur la barrière de mucus intestinal chez le rat: effet du probiotique Lactobacillus farciminis2013Doctoral thesis, monograph (Other academic)
    Abstract [en]

    Background. Despite a large body of literature incriminating mucus alterations in the pathogenesis of Intestinal Bowel Diseases (IBD), structural and physical changes in the mucus layer remain poorly understood in the micro-inflammatory context of Irritable Bowel Syndrome (IBS). Moreover, some probiotic treatments prevent stress-induced intestinal epithelial barrier impairment but little is known about their influence on intestinal mucin structural modifications and mucus properties induced by stress. Thereby, this study aimed at evaluating whether (i) a chronic stress modified the number of gut goblet cells and Muc2 expression and O-glycosylation, (ii) L. farciminis (LF) treatment prevented these alterations and (iii) observed effects were related to the in vivo colonization capacity of LF.

    Main results and conclusions. Water Avoidance Stress (WAS) did not modify neither the number of intestinal goblet cells nor Muc2 expression. Mass Spectrometry analysis demonstrated that O-glycosylation of mucins was strongly affected by WAS, and confirmed in another model of IBS (maternal deprivation model). Under stress conditions, the mucus layer, showed a flattened morphology, probably indicative of a loss in its cohesive properties. The mucus layer alteration was, thus, in relation with epithelial barrier impairment and visceral hypersensitivity. LF administration prevented WAS-induced functional, biochemical and physical changes of mucus. The presence of LF in the ileum and colon was confirmed and we observed that Segmented Filamentous Bacteria (SFB) population was reduced by LF.

    Chronic stress induced functional changes in rats, as well as a shift in mucin O-glycosylation rather than changes in mucin expression, resulting in a loss of mucus layer cohesive properties. These results confirm that LF is a valuable probiotic in the IBS management.

    Methods. IBS Animal model (WAS and maternal deprivation), histological, Mass Spectrometry, Microscopy (Fluorescence, AFM, SEM and TEM), bacterial localization by Fluorescence In Situ Hybridization (FISH), qPCR, intestinal paracellular permeability, visceral sensitivity.

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  • 3. DA SILVA, Stéphanie
    Spatial localization and binding of the probiotic Lactobacillus farciminis to the rat intestinal mucosa: influence of chronic stress2015In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203Article in journal (Refereed)
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  • 4. DA SILVA, Stéphanie
    Stress disrupts intestinal mucus barrier in rats via mucin O-glycosylation shift: prevention by a probiotic treatment.2014In: American Journal of Physiology - Gastrointestinal and Liver Physiology, ISSN 0193-1857, E-ISSN 1522-1547Article in journal (Refereed)
  • 5.
    Da Silva, Stéphanie
    et al.
    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.
    Keita, Åsa V.
    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.
    Mohlin, Sofie
    Translational Cancer Research, Cancer Center at Medicon Village, Lund University, Lund, Sweden.
    Påhlman, Sven
    Translational Cancer Research, Cancer Center at Medicon Village, Lund University, Lund, Sweden.
    Théodorou, Vassilia
    Toxalim UMR 1331 INRA/INP/UPS Neuro-Gastroenterology and Nutrition Unit, Toulouse, France.
    Påhlman, Ingrid
    Albireo AB, Arvid Wallgrens Backe, Gothenburg, Sweden.
    Mattson, Jan P.
    Albireo AB, Arvid Wallgrens Backe, Gothenburg, Sweden.
    Söderholm, Johan D.
    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.
    A novel topical PPARγ agonist induces PPARγ-activity in ulcerative colitis mucosa and prevents and reverses inflammation in induced-colitis models2018In: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 24, no 4, p. 792-805Article in journal (Refereed)
    Abstract [en]

    Background: Peroxisome proliferator-activated receptor-gamma (PPARγ) exerts anti-inflammatory effects and is therefore a potential target in ulcerative colitis (UC). A novel PPARγ agonist (AS002) developed for local action was evaluated ex vivo in biopsies from UC patients and in vivo in mice with low-grade dextran sodium sulfate (DSS)- and trinitrobenzene sulfonic acid (TNBS)-induced colitis.Methods: Colonic biopsies from UC patients (n = 18) and healthy controls (n = 6) were incubated with AS002 or rosiglitazone (positive control) to measure mRNA expression of the PPARγ-responsive gene ADIPOPHILIN and protein levels of UC-related cytokines (enzyme-linked immunosorbent assay). AS002 absorption was determined in the colonic mucosa of UC patients. DSS-colitis mice received PPARγ agonists or vehicle daily by intrarectal administration starting 2 days before induction of colitis (preventive) or from days 3 to 8 (curative). Myeloperoxidase (MPO) and cytokine levels in colonic mucosa were determined. In addition, AS002 effects were studied in TNBS colitis.Results: AS002 displayed an absorption pattern of a lipophilic drug totally metabolized in the mucosa. AS002 and rosiglitazone increased ADIPOPHILIN mRNA expression (3-fold) and decreased TNF-α, IL-1β, and IL-13 levels in human UC biopsies. In DSS, in both preventive and curative treatment and in TNBS colitis, AS002 protected against macroscopic and histological damage and lowered MPO and TNF-α, IL-1β, and IL-13 levels.Conclusions: AS002 triggers anti-inflammatory PPARγ activity in the human colonic mucosa of UC patients and prevents and reverses colitis in mice. Our data suggest that AS002 has potential for topical maintenance treatment of UC, which warrants further studies in vivo in patients.

  • 6.
    Keita, Åsa
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Yakimenko Alkaissi, Lina
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Boström Holm, Elin
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
    Heil, Stéphanie
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Chassaing, Benoit
    Georgia State Univ, GA 30303 USA; Georgia State Univ, GA 30303 USA.
    Darfeuille-Michaud, Arlette
    Univ Auvergne, France.
    McKay, Derek M.
    Univ Calgary, Canada.
    Söderholm, Johan D
    Linköping University, Department of Biomedical and Clinical Sciences, 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.
    Enhanced E. coli LF82 Translocation through the Follicle-associated Epithelium in Crohns Disease is Dependent on Long Polar Fimbriae and CEACAM6 expression, and Increases Paracellular Permeability2020In: Journal of Crohn's & Colitis, ISSN 1873-9946, E-ISSN 1876-4479, Vol. 14, no 2, p. 216-229Article in journal (Refereed)
    Abstract [en]

    Background and Aims: Patients with Crohns disease [CD] harbour an increased number of adherent-invasive E. coli [AIEC]. The strain LF82, identified in the ileal mucosa of CD patients, has been extensively studied for pathogenic mechanisms. However, understanding of the interaction of LF82 with the intestinal mucosa of CD patients is lacking. Methods: Here, we investigated the importance of long polar fimbriae [LPF] type 1 pili and the carcinoembryonic antigen-related cell-adhesion molecule 6 [CEACAM6] for translocation of LF82 in an in vitro model of follicle-associated epithelium [FAE], and in the FAE and villus epithelium [VE] of patients with CD and controls, using Ussing chambers. Results: Significantly greater LF82 passage occurred in the FAE model compared with in the VE Caco-2cl1 mono-culture. Moreover, bacterial translocation was inhibited by either LPF disruption or pre-incubation with anti-CEACAM6 antibody. Tissue mounted in Ussing chambers showed significantly higher LF82 passage in FAE from patients with CD compared with control FAE, that was diminished in LF82 lacking LPF and by blocking host CEACAM6. Interestingly, addition of LF82 to the CD FAE tissues significantly increased paracellular permeability [of (51)Chromium-EDTA] compared with baseline, and the increase was inhibited by anti-CEACAM6. Immunofluorescence and immunoblots showed higher expression of CEACAM6 in FAE of patients with CD compared with in FAE from controls. Conclusions: These data suggest that the FAE of CD patients is a site of vulnerability for invasion by LF82 via a mechanism that requires both bacterial LPF and host CEACAM6. Further, LF82 has the ability to increase paracellular passage through the FAE of patients with CD. These data can help define novel therapeutic targets in CD for the prevention of clinical recurrence.

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  • 7.
    Rincel, Marion
    et al.
    UMR1286, INRA, Nutrition and Integrative Neurobiology (NutriNeuro) Bordeaux France; UMR1286Univ. Bordeaux, Nutrition et Neurobiologie Intégrée Bordeaux France.
    Lépinay, Amandine
    UMR1286, INRA, Nutrition and Integrative Neurobiology (NutriNeuro) Bordeaux France; UMR1286Univ. Bordeaux, Nutrition et Neurobiologie Intégrée Bordeaux France.
    Janthakhin, Yoothana
    UMR1286, INRA, Nutrition and Integrative Neurobiology (NutriNeuro) Bordeaux France; UMR1286 Univ. Bordeaux, Nutrition et Neurobiologie Intégrée Bordeaux France.
    Soudain, Gwenaëlle
    UMR1286, INRA, Nutrition and Integrative Neurobiology (NutriNeuro) Bordeaux France; UMR1286Univ. Bordeaux, Nutrition et Neurobiologie Intégrée Bordeaux France.
    Yvon, Sophie
    Univ. Toulouse, Toulouse, France.
    DA SILVA, Stéphanie
    Univ. Toulouse, Toulouse, France.
    Joffre, Corinne
    UMR1286, INRA, Nutrition and Integrative Neurobiology (NutriNeuro) Bordeaux France; UMR1286 Univ. Bordeaux, Nutrition et Neurobiologie Intégrée Bordeaux France.
    Aubert, Agnes
    UMR1286, INRA, Nutrition and Integrative Neurobiology (NutriNeuro) Bordeaux France; UMR1286 Univ. Bordeaux, Nutrition et Neurobiologie Intégrée Bordeaux France.
    Séré, Alexandra
    UMR1286, INRA, Nutrition and Integrative Neurobiology (NutriNeuro) Bordeaux France; UMR1286 Univ. Bordeaux, Nutrition et Neurobiologie Intégrée Bordeaux France.
    Layé, Sophie
    UMR1286, INRA, Nutrition and Integrative Neurobiology (NutriNeuro) Bordeaux France; UMR1286 Univ. Bordeaux, Nutrition et Neurobiologie Intégrée Bordeaux France.
    Théodorou, Vassilia
    Univ. Toulouse, Toulouse, France.
    Ferreira, Guillaume
    UMR1286, INRA, Nutrition and Integrative Neurobiology (NutriNeuro) Bordeaux France; UMR1286 Univ. Bordeaux, Nutrition et Neurobiologie Intégrée Bordeaux France.
    Darnaudéry, Muriel
    UMR1286, INRA, Nutrition and Integrative Neurobiology (NutriNeuro) Bordeaux France; UMR1286 Univ. Bordeaux, Nutrition et Neurobiologie Intégrée Bordeaux France.
    Maternal high-fat diet and early-life stress differentially modulate spine density and dendritic morphology in the medial prefrontal cortex of juvenile and adult rats.2018In: Brain Structure and Function, ISSN 1863-2653, E-ISSN 1863-2661, Vol. 223, no 2, p. 883-895Article in journal (Refereed)
    Abstract [en]

    The medial prefrontal cortex (mPFC) is a key area for the regulation of numerous brain functions including stress response and cognitive processes. This brain area is also particularly affected by adversity during early life. Using an animal model in rats, we recently demonstrated that maternal exposure to a high-fat diet (HFD) prevents maternal separation (MS)-induced gene expression alterations in the developing PFC and attenuates several long-term deleterious behavioral effects of MS. In the present study, we ask whether maternal HFD could protect mPFC neurons of pups exposed to early life stress by examining dendritic morphology and spine density in juvenile [postnatal day (PND) 21] and adult rats submitted to MS. Dams were fed either a control or an HFD throughout gestation and lactation, and pups were submitted to MS from PND2 to PND14. We report that maternal HFD prevents MS-induced spine loss at PND21 and dendritic atrophy at adulthood. Furthermore, we show in adult MS rats that PFC-dependent memory extinction deficits are prevented by maternal HFD. Finally, perinatal HFD exposure reverses gut leakiness following stress in pups and seems to exert an anti-stress effect in dams. Overall, our work demonstrates that maternal HFD affects the developing brain and suggests that nutrition, possibly through gut–brain interactions, could modulate mPFC sensitivity to early stress.

  • 8.
    Signoret, Carine
    et al.
    Linköping University, Department of Behavioural Sciences and Learning, Disability Research. Linköping University, Faculty of Arts and Sciences. Linköping University, The Swedish Institute for Disability Research.
    Ng, Hoi Ning, Elaine
    Linköping University, Department of Behavioural Sciences and Learning, Disability Research. Linköping University, Faculty of Arts and Sciences. Linköping University, The Swedish Institute for Disability Research.
    da Silva, Stéphanie
    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.
    Tack, Ayco
    Stockholm University, Stockholm, Sweden.
    Voss, Ulrikke
    Lund University, Lund, Sweden.
    Lidö, Helga H.
    The Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
    Patthey, Cédric
    Umeå University, Umeå, Sweden; .
    Ericsson, Madelene
    Umeå University, Umeå, Sweden.
    Hadrévi, Jenny
    Umeå University, Umeå, Sweden.
    Balachandran, Chanchal
    Linköping University, Department of Management and Engineering, The Institute for Analytical Sociology, IAS. Linköping University, Faculty of Arts and Sciences.
    Well-Being of Early-Career Researchers: Insights from a Swedish Survey2019In: Higher Education Policy, ISSN 0952-8733, E-ISSN 1740-3863, Vol. 32, no 2, p. 273-296Article in journal (Refereed)
    Abstract [en]

    Several studies have documented the importance of optimal work situation and the general well-being of early-career researchers (ECRs) for enhancing the academic performance of universities. Yet, most studies focused on specific categories of ECRs, or on specific academic disciplines as well as on specific outcomes. With this study, we recognize the need for a broader sample encompassing different categories of ECRs across academic disciplines. In a national survey of Swedish universities, the National Junior Faculty of Sweden (NJF) collected data from ECRs in order to study the influence of work situation and well-being on perceived scientific environment. We observed that work situation and well-being are interdependent and jointly influence each other in shaping the conditions for ideal scientific environment. Importantly, we employ structural equation model (SEM) analysis to account for the endogenous relationship between work situation and personal well-being in predicting perceived scientific environment. Results from SEM indicate that support from the university, work time management, job clarity, contract length and quality of life satisfaction were related to the perceived possibility of conducting the best science. Our research also highlighted individual differences across demographic factors and contract length in the perceived work situation and the possibility of conducting the best science. © 2018 International Association of Universities

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