Short Chain Fatty Acids (SCFAs)-Mediated Gut Epithelial and Immune Regulation and Its Relevance for Inflammatory Bowel Diseases

Ulcerative colitis (UC) and Crohn's disease (CD), collectively known as Inflammatory Bowel Diseases (IBD), are caused by a complex interplay between genetic, immunologic, microbial and environmental factors. Dysbiosis of the gut microbiome is increasingly considered to be causatively related to...

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Vydané v:Frontiers in immunology Ročník 10; s. 277
Hlavní autori: Parada Venegas, Daniela, De la Fuente, Marjorie K., Landskron, Glauben, González, María Julieta, Quera, Rodrigo, Dijkstra, Gerard, Harmsen, Hermie J. M., Faber, Klaas Nico, Hermoso, Marcela A.
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Switzerland Frontiers Media S.A 11.03.2019
Predmet:
dysbiosis
IBD
IECs
immune cells
Immunology
intestinal mucosa
SCFAs
SCFAs
immune cells
IBD
intestinal mucosa
IECs
dysbiosis
ISSN:1664-3224, 1664-3224
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Shrnutí:Ulcerative colitis (UC) and Crohn's disease (CD), collectively known as Inflammatory Bowel Diseases (IBD), are caused by a complex interplay between genetic, immunologic, microbial and environmental factors. Dysbiosis of the gut microbiome is increasingly considered to be causatively related to IBD and is strongly affected by components of a Western life style. Bacteria that ferment fibers and produce short chain fatty acids (SCFAs) are typically reduced in mucosa and feces of patients with IBD, as compared to healthy individuals. SCFAs, such as acetate, propionate and butyrate, are important metabolites in maintaining intestinal homeostasis. Several studies have indeed shown that fecal SCFAs levels are reduced in active IBD. SCFAs are an important fuel for intestinal epithelial cells and are known to strengthen the gut barrier function. Recent findings, however, show that SCFAs, and in particular butyrate, also have important immunomodulatory functions. Absorption of SCFAs is facilitated by substrate transporters like MCT1 and SMCT1 to promote cellular metabolism. Moreover, SCFAs may signal through cell surface G-protein coupled receptors (GPCRs), like GPR41, GPR43, and GPR109A, to activate signaling cascades that control immune functions. Transgenic mouse models support the key role of these GPCRs in controlling intestinal inflammation. Here, we present an overview of microbial SCFAs production and their effects on the intestinal mucosa with specific emphasis on their relevance for IBD. Moreover, we discuss the therapeutic potential of SCFAs for IBD, either applied directly or by stimulating SCFAs-producing bacteria through pre- or probiotic approaches.
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This article was submitted to Mucosal Immunity, a section of the journal Frontiers in Immunology
Edited by: Ed C. Lavelle, Trinity College Dublin, Ireland
Reviewed by: Sukanya Raghavan, University of Gothenburg, Sweden; Craig Patrick McEntee, University of Manchester, United Kingdom
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2019.00277