| The bacterial signal indole increases epithelial-cell tight-junction resistance and attenuates indicators of inflammation. | |
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MedLine Citation:
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PMID: 19966295 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Interkingdom signaling is established in the gastrointestinal tract in that human hormones trigger responses in bacteria; here, we show that the corollary is true, that a specific bacterial signal, indole, is recognized as a beneficial signal in intestinal epithelial cells. Our prior work has shown that indole, secreted by commensal Escherichia coli and detected in human feces, reduces pathogenic E. coli chemotaxis, motility, and attachment to epithelial cells. However, the effect of indole on intestinal epithelial cells is not known. Because intestinal epithelial cells are likely to be exposed continuously to indole, we hypothesized that indole may be beneficial for these cells, and investigated changes in gene expression with the human enterocyte cell line HCT-8 upon exposure to indole. Exposure to physiologically relevant amounts of indole increased expression of genes involved in strengthening the mucosal barrier and mucin production, which were consistent with an increase in the transepithelial resistance of HCT-8 cells. Indole also decreased TNF-alpha-mediated activation of NF-kappaB, expression of the proinflammatory chemokine IL-8, and the attachment of pathogenic E. coli to HCT-8 cells, as well as increased expression of the antiinflammatory cytokine IL-10. The changes in transepithelial resistance and NF-kappaB activation were specific to indole: other indole-like molecules did not elicit a similar response. Our results are similar to those observed with probiotic strains and suggest that indole could be important in the intestinal epithelial cells response to gastrointestinal tract pathogens. |
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Authors:
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Tarun Bansal; Robert C Alaniz; Thomas K Wood; Arul Jayaraman |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S. Date: 2009-12-04 |
Journal Detail:
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Title: Proceedings of the National Academy of Sciences of the United States of America Volume: 107 ISSN: 1091-6490 ISO Abbreviation: Proc. Natl. Acad. Sci. U.S.A. Publication Date: 2010 Jan |
Date Detail:
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Created Date: 2010-01-18 Completed Date: 2010-03-09 Revised Date: 2013-05-31 |
Medline Journal Info:
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Nlm Unique ID: 7505876 Medline TA: Proc Natl Acad Sci U S A Country: United States |
Other Details:
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Languages: eng Pagination: 228-33 Citation Subset: IM |
Affiliation:
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Artie McFerrin Department of Chemical Engineering, Texas A&M University, College Station, TX 77843, USA. |
| Data Bank Information | |
Bank Name/Acc. No.:
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GEO/GSE14379 |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Bacteria
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chemistry,
metabolism* Cell Line Chemokines / immunology Cytokines / immunology Epithelial Cells / cytology, metabolism* Humans Indoles / metabolism* Inflammation / metabolism* Microarray Analysis NF-kappa B / genetics, metabolism Recombinant Fusion Proteins / genetics, metabolism Signal Transduction / physiology* Tight Junctions / metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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R01 EB003872/EB/NIBIB NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Chemokines; 0/Cytokines; 0/Indoles; 0/NF-kappa B; 0/Recombinant Fusion Proteins; 8724FJW4M5/indole |
| Comments/Corrections | |
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