PloS one, 2007-12, Vol.2 (12), p.e1308-e1308
2007
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- Autor(en) / Beteiligte
- Titel
- Probiotic Escherichia coli Nissle 1917 inhibits leaky gut by enhancing mucosal integrity
- Ist Teil von
- PloS one, 2007-12, Vol.2 (12), p.e1308-e1308
- Ort / Verlag
- United States: Public Library of Science
- Erscheinungsjahr
- 2007
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- 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). 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. 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.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1932-6203eISSN: 1932-6203DOI: 10.1371/journal.pone.0001308Titel-ID: cdi_plos_journals_1950342709
- Format
- –
- Schlagworte
- Absorptivity, Animal models, Animals, Base Sequence, Blotting, Western, Body weight, Colitis, Colitis - physiopathology, Colitis - therapy, Colon, Colonization, Crohns disease, Cytokines, Dextran, Dextrans, Diarrhea, Disruption, DNA Primers, E coli, Endocrinology, Epithelial cells, Escherichia coli, Experiments, Fatty acids, Feces, Female, Fluorescent Antibody Technique, Gastroenterology, Gastroenterology and Hepatology/Inflammatory Bowel Disease, Gastrointestinal diseases, Gene expression, Germ-Free Life, Germfree, Gnotobiotic, Health aspects, Hematology, Hepatology, HIV, Human immunodeficiency virus, In vivo methods and tests, Infection, Infections, Infectious Diseases/Gastrointestinal Infections, Infiltration, Inflammatory bowel disease, Inflammatory bowel diseases, Intestinal Mucosa - physiopathology, Intestine, Laboratory animals, Leukocytes, Medical schools, Membrane permeability, Metabolites, Mice, Mice, Inbred BALB C, Microbiology/Immunity to Infections, Microbiology/Medical Microbiology, Microorganisms, mRNA, Mucosa, Oncology, Oral administration, Permeability, Probiotics, Proteins, RNA, Rodents, Sodium, Sodium sulfate, Sulfates, Weight reduction, Zonula occludens-1 protein