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Lactobacillus reuteri prevents colitis by reducing P-selectin-associated leukocyte- and platelet-endothelial cell interactions
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology, Integrative Physiology.
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2009 (English)In: American Journal of Physiology - Gastrointestinal and Liver Physiology, ISSN 0193-1857, E-ISSN 1522-1547, Vol. 296, no 3, G534-G542 p.Article in journal (Refereed) Published
Abstract [en]

Recent findings indicate that dextran sodium sulfate (DSS)-induced colitis is associated with a prothrombogenic phenotype, with P-selectin playing a major role in platelet recruitment. It has been suggested that probiotics may ameliorate colonic inflammation. We therefore investigated how treatment with Lactobacillus reuteri influenced P-selectin expression, leukocyte and platelet endothelial cell interactions, and colitis severity in DSS-treated rats. Rats were divided into the following four groups: nontreated, DSS treated (5% in drinking water for 9 days), L. reuteri, and L. reuteri and DSS treated. The rats were anesthetized with Inactin (120 mg/kg ip), and the dual radiolabeled monoclonal antibody technique was used to quantify P-selectin expression. Leukocyte-endothelial and platelet-endothelial cell interactions were studied in colonic venules with intravital microscopy. Colitis severity was assessed using a disease activity index. Disease activity index increased, as did the expression of P-selectin in the entire colon after DSS treatment, but both were reduced to control levels with L. reuteri pretreatment. The increased platelet- and leukocyte-endothelial cell interactions after DSS treatment were abolished by pretreatment with L. reuteri. L. reuteri protects against DSS-induced colitis in rats. The protection is associated with reduced P-selectin expression and a decrease in leukocyte- and platelet-endothelial cell interactions.

Place, publisher, year, edition, pages
2009. Vol. 296, no 3, G534-G542 p.
Keyword [en]
dextran sulfate sodium, disease activity index
National Category
Medical and Health Sciences Medical and Health Sciences Physiology
Identifiers
URN: urn:nbn:se:uu:diva-104355DOI: 10.1152/ajpgi.90470.2008ISI: 000263900800010PubMedID: 19147805OAI: oai:DiVA.org:uu-104355DiVA: diva2:219685
Available from: 2009-05-28 Created: 2009-05-28 Last updated: 2014-11-05Bibliographically approved
In thesis
1. Microcirculation, Mucus and Microbiota in Inflammatory Bowel Disease
Open this publication in new window or tab >>Microcirculation, Mucus and Microbiota in Inflammatory Bowel Disease
2010 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Inflammatory bowel diseases, (IBD), are a group of chronic disorders of the gastro-intestinal tract, and include Crohn’s disease (CD) and Ulcerative Colitis (UC). The pathogenesis is not known, but involves at least in part a loss of tolerance towards the commensal colonic microbiota. In this thesis, we show in animal models of CD and UC that the colonic mucosal blood flow increased compared to healthy animals. This blood flow increase is due to an up regulation of endothelial nitric oxide synthase (NOS). Further, we show in the UC model that the thickness of the firmly adherent colonic mucus layer increased compared to healthy animals. This increase is due to an up regulation of inducible NOS in the epithelium. Both the blood flow and mucus thickness increase appear to be protective mechanisms.  We demonstrate that the firmly adherent colonic mucus layer acts as a partial barrier towards luminal bacteria. In the UC model, this barrier is destroyed, causing increased bacterial translocation. The adhesion molecule P-selectin was up regulated in the UC model, leading to increased interactions between leukocytes and the endothelium, but also increased interactions between platelets and the endothelium. This indicates that not only leukocytes, but also platelets are involved in colonic inflammation. The addition of the probiotic bacterial strain Lactobacillus reuteri prevented disease by normalizing P-selectin levels and endothelial interactions with leukocytes and platelets. Lactobacillus reuteri also decreased bacterial translocation over the epithelium. In summary, this thesis highlights the importance of colonic barrier functions, and investigates the role of the microbiota in experimental IBD.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2010. 59 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 516
Keyword
inflammatory bowel diseases, experimental colitis, DSS, TNBS, colonic mucosal blood flow, laser-doppler flowmetry, colonic mucus thickness, MUC2, colonic mucosal barrier function, iNOS, eNOS, probiotics, Lactobacilli, Lactobacillus reuteri, colonic microbiota, T-RFLP, bacterial translocation, intravital microscopy, P-selectin, leukocyte recruitment, platelet recruitment
National Category
Physiology
Research subject
Physiology
Identifiers
urn:nbn:se:uu:diva-112718 (URN)978-91-554-7710-3 (ISBN)
Public defence
2010-03-06, Auditorium Minus, Museum Gustavianum, Akademigatan 3, Uppsala, 13:15 (Swedish)
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Supervisors
Available from: 2010-02-12 Created: 2010-01-19 Last updated: 2010-02-12Bibliographically approved

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Phillipson, MiaHolm, Lena

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