Show simple item record

dc.contributor.authorM. Maslowski, Kendle
dc.contributor.authorT. Vieira, Angelica
dc.contributor.authorNg, Aylwin
dc.contributor.authorKranich, Jan
dc.contributor.authorKranich, Jan
dc.contributor.authorSierro, Frederic
dc.contributor.authorYu, Di
dc.contributor.authorC. Schilter, Heidi
dc.contributor.authorS. Rolph, Michael
dc.contributor.authorMackay, Fabienne
dc.contributor.authorArtis, David
dc.contributor.authorJ. Xavier, Ramnik
dc.contributor.authorM. Teixeira, Mauro
dc.contributor.authorMackay, Charles R.
dc.date.accessioned2017-05-03T16:02:15Z
dc.date.available2017-05-03T16:02:15Z
dc.date.issued2009
dc.date.modified2011-03-31T04:46:42Z
dc.identifier.issn00280836
dc.identifier.doi10.1038/nature08530
dc.identifier.urihttp://hdl.handle.net/10072/37877
dc.description.abstractThe 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 diseases1, 2. 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 3, and a concurrent reduction in SCFAs4. Moreover, increased intake of fermentable dietary fibre, or SCFAs, seems to be clinically beneficial in the treatment of colitis5, 6, 7, 8, 9. SCFAs bind the G-protein-coupled receptor 43 (GPR43, also known as FFAR2)10, 11, 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.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherNature Publishing Group
dc.publisher.placeUnited Kingdom
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom1282
dc.relation.ispartofpageto1286
dc.relation.ispartofjournalNature
dc.relation.ispartofvolume461
dc.rights.retentionY
dc.subject.fieldofresearchCellular Immunology
dc.subject.fieldofresearchcode110704
dc.titleRegulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR43
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.date.issued2009
gro.hasfulltextNo Full Text
gro.griffith.authorRolph, Michael S.


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

  • Journal articles
    Contains articles published by Griffith authors in scholarly journals.

Show simple item record