Journal ArticleDOI
Short-chain fatty acids activate GPR41 and GPR43 on intestinal epithelial cells to promote inflammatory responses in mice.
TLDR
GPR41 and GPR43 mice had reduced inflammatory responses after administration of ethanol or TNBS compared with control mice, and had a slower immune response against C rodentium infection, clearing the bacteria more slowly.About:
This article is published in Gastroenterology.The article was published on 2013-08-01. It has received 694 citations till now. The article focuses on the topics: Chemokine & Cytokine.read more
Citations
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Journal ArticleDOI
Short Chain Fatty Acids (SCFAs)-Mediated Gut Epithelial and Immune Regulation and Its Relevance for Inflammatory Bowel Diseases.
Daniela Parada Venegas,Marjorie De la Fuente,Glauben Landskron,María-Julieta González,Rodrigo Quera,Gerard Dijkstra,Hermie J. M. Harmsen,Klaas Nico Faber,Marcela A. Hermoso +8 more
TL;DR: An overview of microbial SCFAs production and their effects on the intestinal mucosa with specific emphasis on their relevance for Inflammatory Bowel Diseases is presented and the therapeutic potential ofSCFAs for IBD is discussed.
Journal ArticleDOI
Regulation of immune cell function by short-chain fatty acids
Renan Corrêa-Oliveira,José Luís Fachi,Aline Vieira,Fabio Takeo Sato,Marco Aurélio Ramirez Vinolo +4 more
TL;DR: The aim of this review is to present a clear and updated description of the effects of the SCFAs derived from bacteria on host immune system, as well as the molecular mechanisms involved on them.
Journal ArticleDOI
Short-chain fatty acids induce both effector and regulatory T cells by suppression of histone deacetylases and regulation of the mTOR-S6K pathway.
Jeongho Park,Myunghoo Kim,Seung Goo Kang,Amber H. Jannasch,Bruce A. Cooper,John A. Patterson,Chang H. Kim +6 more
TL;DR: It is reported that SCFAs can directly promote T-cell differentiation into T cells producing interleukin-17, interferon-γ, and/or IL-10 depending on cytokine milieu.
Journal ArticleDOI
Tuft cells, taste-chemosensory cells, orchestrate parasite type 2 immunity in the gut
Michael R. Howitt,Sydney Lavoie,Monia Michaud,Arthur M. Blum,Sara V. Tran,Joel V. Weinstock,Carey Ann Gallini,Kevin Redding,Robert F. Margolskee,Lisa C. Osborne,David Artis,Wendy S. Garrett,Wendy S. Garrett +12 more
TL;DR: It is shown that tuft cells, which are taste-chemosensory epithelial cells, accumulate during parasite colonization and infection and are identified as critical sentinels in the gut epithelium that promote type 2 immunity in response to intestinal parasites.
Journal ArticleDOI
Dietary Fatty Acids Directly Impact Central Nervous System Autoimmunity via the Small Intestine
Aiden Haghikia,Stefanie Jörg,Alexander Duscha,Johannes Berg,Arndt Manzel,Anne Waschbisch,Anna Hammer,De-Hyung Lee,Caroline May,Nicola Wilck,András Balogh,Annika I. Ostermann,Nils Helge Schebb,Denis A. Akkad,Diana A. Grohme,Markus Kleinewietfeld,Stefan Kempa,Jan Thöne,Seray Demir,Dominik N. Müller,Ralf Gold,Ralf A. Linker +21 more
TL;DR: Dietary long-chain fatty acids enhanced differentiation and proliferation of T helper 1 and/or Th17 cells and impaired their intestinal sequestration via p38-MAPK pathway and dietary short-chain FAs expanded gut T regulatory (Treg) cells by suppression of the JNK1 and p38 pathway.
References
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Journal ArticleDOI
Regulation of inflammatory responses by gut microbiota and chemoattractant receptor GPR43
Kendle M. Maslowski,Angélica T. Vieira,Angélica T. Vieira,Aylwin Ng,Jan Kranich,Frederic Sierro,Di Yu,Heidi C. Schilter,Heidi C. Schilter,Michael S. Rolph,Fabienne Mackay,Fabienne Mackay,David Artis,Ramnik J. Xavier,Ramnik J. Xavier,Mauro M. Teixeira,Charles R. Mackay +16 more
TL;DR: It is shown that SCFA–GPR43 interactions profoundly affect inflammatory responses, and GPR43 binding of SCFAs potentially provides a molecular link between diet, gastrointestinal bacterial metabolism, and immune and inflammatory responses.
Journal ArticleDOI
The Orphan G Protein-coupled Receptors GPR41 and GPR43 Are Activated by Propionate and Other Short Chain Carboxylic Acids
Andrew J. Brown,Susan M. Goldsworthy,Ashley A. Barnes,Michelle M. Eilert,Lili Tcheang,Dion A. Daniels,Alison I. Muir,Mark J. Wigglesworth,Ian Kinghorn,Neil J. Fraser,Nicholas B. Pike,Jay C. Strum,Klaudia Steplewski,Paul R. Murdock,Julie C. Holder,Fiona H. Marshall,Philip G. Szekeres,Shelagh Wilson,Diane M. Ignar,Steve M. Foord,Alan Wise,Simon J. Dowell +21 more
TL;DR: GPR41 was expressed primarily in adipose tissue, whereas the highest levels of GPR43 were found in immune cells, and was activated by similar ligands but with differing specificity for carbon chain length, with pentanoate being the most potent agonist.
Journal ArticleDOI
Chemically induced mouse models of intestinal inflammation.
TL;DR: In this paper, the authors provide protocols for establishing murine 2,4,6-trinitro benzene sulfonic acid (TNBS)-, oxazolone- and both acute and chronic dextran sodium sulfate (DSS) colitis, the most widely used chemically induced models of intestinal inflammation.
Journal ArticleDOI
Effects of the gut microbiota on host adiposity are modulated by the short-chain fatty-acid binding G protein-coupled receptor, Gpr41
Buck S. Samuel,Abdullah Shaito,Toshiyuki Motoike,Federico E. Rey,Fredrik Bäckhed,Fredrik Bäckhed,Jill K. Manchester,Robert E. Hammer,S. Clay Williams,Jan R. Crowley,Masashi Yanagisawa,Jeffrey I. Gordon +11 more
TL;DR: Functional genomic, biochemical, and physiologic studies reveal that Gpr41 is a regulator of host energy balance through effects that are dependent upon the gut microbiota.
Journal ArticleDOI
Functional characterization of human receptors for short chain fatty acids and their role in polymorphonuclear cell activation.
Emmanuel Le Poul,Cecile Loison,Sofie Struyf,Jean-Yves Springael,Vincent Lannoy,Marie-Eve Decobecq,Stéphane Brézillon,Vincent Dupriez,Gilbert Vassart,Jozef Van Damme,Marc Parmentier,Michel Detheux +11 more
TL;DR: The pharmacology of GPR43 matches indeed the effects of SCFAs on neutrophils, in terms of intracellular Ca2+ release and chemotaxis, and might constitute a target allowing us to modulate immune responses in these pathological situations.
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