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dc.contributor.authorUkena, Sya N
dc.contributor.authorSingh, Anurag
dc.contributor.authorDringenberg, Ulrike
dc.contributor.authorEngelhardt, Regina
dc.contributor.authorSeidler, Ursula
dc.contributor.authorHansen, Wiebke
dc.contributor.authorBleich, André
dc.contributor.authorBruder, Dunja
dc.contributor.authorFranzke, Anke
dc.contributor.authorRogler, Gerhard
dc.contributor.authorSuerbaum, Sebastian
dc.contributor.authorBuer, Jan
dc.contributor.authorGunzer, Florian
dc.contributor.authorWestendorf, Astrid M
dc.date.accessioned2010-03-12T09:20:52Z
dc.date.available2010-03-12T09:20:52Z
dc.date.issued2007
dc.identifier.citationProbiotic Escherichia coli Nissle 1917 inhibits leaky gut by enhancing mucosal integrity. 2007, 2 (12):e1308 PLoS ONEen
dc.identifier.issn1932-6203
dc.identifier.pmid18074031
dc.identifier.doi10.1371/journal.pone.0001308
dc.identifier.urihttp://hdl.handle.net/10033/94153
dc.description.abstractBACKGROUND: Probiotics are proposed to positively modulate the intestinal epithelial barrier formed by intestinal epithelial cells (IECs) and intercellular junctions. Disruption of this border alters paracellular permeability and is a key mechanism for the development of enteric infections and inflammatory bowel diseases (IBDs). METHODOLOGY AND PRINCIPAL FINDINGS: To study the in vivo effect of probiotic Escherichia coli Nissle 1917 (EcN) on the stabilization of the intestinal barrier under healthy conditions, germfree mice were colonized with EcN or K12 E. coli strain MG1655. IECs were isolated and analyzed for gene and protein expression of the tight junction molecules ZO-1 and ZO-2. Then, in order to analyze beneficial effects of EcN under inflammatory conditions, the probiotic was orally administered to BALB/c mice with acute dextran sodium sulfate (DSS) induced colitis. Colonization of gnotobiotic mice with EcN resulted in an up-regulation of ZO-1 in IECs at both mRNA and protein levels. EcN administration to DSS-treated mice reduced the loss of body weight and colon shortening. In addition, infiltration of the colon with leukocytes was ameliorated in EcN inoculated mice. Acute DSS colitis did not result in an anion secretory defect, but abrogated the sodium absorptive function of the mucosa. Additionally, intestinal barrier function was severely affected as evidenced by a strong increase in the mucosal uptake of Evans blue in vivo. Concomitant administration of EcN to DSS treated animals resulted in a significant protection against intestinal barrier dysfunction and IECs isolated from these mice exhibited a more pronounced expression of ZO-1. CONCLUSION AND SIGNIFICANCE: This study convincingly demonstrates that probiotic EcN is able to mediate up-regulation of ZO-1 expression in murine IECs and confer protection from the DSS colitis-associated increase in mucosal permeability to luminal substances.
dc.language.isoenen
dc.subject.meshAnimalsen
dc.subject.meshBase Sequenceen
dc.subject.meshBlotting, Westernen
dc.subject.meshColitisen
dc.subject.meshDNA Primersen
dc.subject.meshEscherichia colien
dc.subject.meshFemaleen
dc.subject.meshFluorescent Antibody Techniqueen
dc.subject.meshGerm-Free Lifeen
dc.subject.meshIntestinal Mucosaen
dc.subject.meshMiceen
dc.subject.meshMice, Inbred BALB Cen
dc.subject.meshProbioticsen
dc.titleProbiotic Escherichia coli Nissle 1917 inhibits leaky gut by enhancing mucosal integrity.en
dc.typeArticleen
dc.contributor.departmentDepartment of Mucosal Immunity, Helmholtz Centre for Infection Research, Braunschweig, Germany.en
dc.identifier.journalPloS oneen
refterms.dateFOA2018-06-13T09:10:25Z
html.description.abstractBACKGROUND: Probiotics are proposed to positively modulate the intestinal epithelial barrier formed by intestinal epithelial cells (IECs) and intercellular junctions. Disruption of this border alters paracellular permeability and is a key mechanism for the development of enteric infections and inflammatory bowel diseases (IBDs). METHODOLOGY AND PRINCIPAL FINDINGS: To study the in vivo effect of probiotic Escherichia coli Nissle 1917 (EcN) on the stabilization of the intestinal barrier under healthy conditions, germfree mice were colonized with EcN or K12 E. coli strain MG1655. IECs were isolated and analyzed for gene and protein expression of the tight junction molecules ZO-1 and ZO-2. Then, in order to analyze beneficial effects of EcN under inflammatory conditions, the probiotic was orally administered to BALB/c mice with acute dextran sodium sulfate (DSS) induced colitis. Colonization of gnotobiotic mice with EcN resulted in an up-regulation of ZO-1 in IECs at both mRNA and protein levels. EcN administration to DSS-treated mice reduced the loss of body weight and colon shortening. In addition, infiltration of the colon with leukocytes was ameliorated in EcN inoculated mice. Acute DSS colitis did not result in an anion secretory defect, but abrogated the sodium absorptive function of the mucosa. Additionally, intestinal barrier function was severely affected as evidenced by a strong increase in the mucosal uptake of Evans blue in vivo. Concomitant administration of EcN to DSS treated animals resulted in a significant protection against intestinal barrier dysfunction and IECs isolated from these mice exhibited a more pronounced expression of ZO-1. CONCLUSION AND SIGNIFICANCE: This study convincingly demonstrates that probiotic EcN is able to mediate up-regulation of ZO-1 expression in murine IECs and confer protection from the DSS colitis-associated increase in mucosal permeability to luminal substances.


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