Regulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR43
Nature, ISSN: 0028-0836, Vol: 461, Issue: 7268, Page: 1282-1286
2009
- 2,579Citations
- 2,162Captures
- 10Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations2,579
- Citation Indexes2,572
- 2,572
- CrossRef2,181
- 1,362
- Patent Family Citations7
- Patent Families7
- Captures2,162
- Readers2,162
- 2,162
- Mentions10
- News Mentions7
- News7
- References2
- Wikipedia2
- Blog Mentions1
- Blog1
Most Recent News
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Article Description
The immune system responds to pathogens by a variety of pattern recognition molecules such as the Toll-like receptors (TLRs), which promote recognition of dangerous foreign pathogens. However, recent evidence indicates that normal intestinal microbiota might also positively influence immune responses, and protect against the development of inflammatory diseases. One of these elements may be short-chain fatty acids (SCFAs), which are produced by fermentation of dietary fibre by intestinal microbiota. A feature of human ulcerative colitis and other colitic diseases is a change in healthy microbiota such as Bifidobacterium and Bacteriodes, and a concurrent reduction in SCFAs. Moreover, increased intake of fermentable dietary fibre, or SCFAs, seems to be clinically beneficial in the treatment of colitis. SCFAs bind the G-protein-coupled receptor 43 (GPR43, also known as FFAR2), and here we show that SCFA-GPR43 interactions profoundly affect inflammatory responses. Stimulation of GPR43 by SCFAs was necessary for the normal resolution of certain inflammatory responses, because GPR43-deficient (Gpr43-/-) mice showed exacerbated or unresolving inflammation in models of colitis, arthritis and asthma. This seemed to relate to increased production of inflammatory mediators by Gpr43-/-immune cells, and increased immune cell recruitment. Germ-free mice, which are devoid of bacteria and express little or no SCFAs, showed a similar dysregulation of certain inflammatory responses. GPR43 binding of SCFAs potentially provides a molecular link between diet, gastrointestinal bacterial metabolism, and immune and inflammatory responses. © 2009 Macmillan Publishers Limited. All rights reserved.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=70350666634&origin=inward; http://dx.doi.org/10.1038/nature08530; http://www.ncbi.nlm.nih.gov/pubmed/19865172; https://www.nature.com/articles/nature08530; https://facultyopinions.com/prime/1166591#eval627600; http://dx.doi.org/10.3410/f.1166591.627600; https://facultyopinions.com/prime/1166591#eval629046; http://dx.doi.org/10.3410/f.1166591.629046; https://facultyopinions.com/prime/1166591#eval3210054; http://dx.doi.org/10.3410/f.1166591.3210054; https://dx.doi.org/10.1038/nature08530; http://europepmc.org/abstract/med/19865172; http://europepmc.org/articles/PMC3256734; http://f1000.com/1166591#eval627600; http://f1000.com/1166591#eval629046; http://f1000.com/1166591#eval3210054
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