Live probiotics protect intestinal epithelial cells from the effects of infection with enteroinvasive Escherichia coli (EIEC)
Background: The colonic epithelium maintains a life long reciprocally beneficial interaction with the colonic microbiota. Disruption is associated with mucosal injury. Aims: We hypothesised that probiotics may limit epithelial damage induced by enteroinvasive pathogens, and promote restitution. Meth...
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Published in | Gut Vol. 52; no. 7; pp. 988 - 997 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
London
BMJ Publishing Group Ltd and British Society of Gastroenterology
01.07.2003
BMJ BMJ Publishing Group LTD Copyright 2003 by Gut |
Subjects | |
Online Access | Get full text |
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Summary: | Background: The colonic epithelium maintains a life long reciprocally beneficial interaction with the colonic microbiota. Disruption is associated with mucosal injury. Aims: We hypothesised that probiotics may limit epithelial damage induced by enteroinvasive pathogens, and promote restitution. Methods: Human intestinal epithelial cell lines (HT29/cl.19A and Caco-2) were exposed to enteroinvasive Escherichia coli (EIEC 029:NM), and/or probiotics (Streptococcus thermophilus (ST), ATCC19258, and Lactobacillus acidophilus (LA), ATCC4356). Infected cells and controls were assessed for transepithelial resistance, chloride secretory responses, alterations in cytoskeletal and tight junctional proteins, and responses to epidermal growth factor (EGF) stimulation. Results: Exposure of cell monolayers to live ST/LA, but not to heat inactivated ST/LA, significantly limited adhesion, invasion, and physiological dysfunction induced by EIEC. Antibiotic killed ST/LA reduced adhesion somewhat but were less effective in limiting the consequences of EIEC invasion of cell monolayers. Furthermore, live ST/LA alone increased transepithelial resistance, contrasting markedly with the fall in resistance evoked by EIEC infection, which could also be blocked by live ST/LA. The effect of ST/LA on resistance was accompanied by maintenance (actin, ZO-1) or enhancement (actinin, occludin) of cytoskeletal and tight junctional protein phosphorylation. ST/LA had no effect on chloride secretion by themselves but reversed the increase in basal secretion evoked by EIEC. EIEC also reduced the ability of EGF to activate its receptor, which was reversed by ST/LA. Conclusions: Live ST/LA interact with intestinal epithelial cells to protect them from the deleterious effect of EIEC via mechanisms that include, but are not limited to, interference with pathogen adhesion and invasion. Probiotics likely also enhance the barrier function of naïve epithelial cells not exposed to any pathogen. |
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Bibliography: | PMID:12801956 istex:01DD1739DC45E8F0752B1008EBBFA428501A5407 Correspondence to: Dr S Resta-Lenert, UCSD Medical Center 8414, 200 West Arbor Drive, San Diego, CA 92103, USA; srestalenert@ucsd.edu ark:/67375/NVC-FL7177JD-9 href:gutjnl-52-988.pdf local:0520988 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Correspondence to: Dr S Resta-Lenert, UCSD Medical Center 8414, 200 West Arbor Drive, San Diego, CA 92103, USA; srestalenert@ucsd.edu |
ISSN: | 0017-5749 1468-3288 1458-3288 |
DOI: | 10.1136/gut.52.7.988 |