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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Published in:	Frontiers in immunology Vol. 10; p. 277
Main Authors:	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.
Format:	Journal Article
Language:	English
Published:	Switzerland Frontiers Media S.A 11.03.2019
Subjects:	dysbiosis IBD IECs immune cells Immunology intestinal mucosa SCFAs SCFAs immune cells IBD intestinal mucosa IECs dysbiosis
ISSN:	1664-3224, 1664-3224
Online Access:	Get full text
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Abstract	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.
AbstractList	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. 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.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.
Author	Landskron, Glauben Dijkstra, Gerard Hermoso, Marcela A. González, María Julieta Faber, Klaas Nico Quera, Rodrigo Parada Venegas, Daniela Harmsen, Hermie J. M. De la Fuente, Marjorie K.
AuthorAffiliation	6 Department of Laboratory Medicine, University Medical Center Groningen, University of Groningen , Groningen , Netherlands 5 Department of Medical Microbiology, University of Groningen, University Medical Center Groningen , Groningen , Netherlands 3 Program of Cell and Molecular Biology, Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile , Santiago , Chile 1 Laboratory of Innate Immunity, Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile , Santiago , Chile 2 Department of Gastroenterology and Hepatology, University of Groningen, University Medical Center Groningen , Groningen , Netherlands 4 Inflammatory Bowel Diseases Program, Department of Gastroenterology, Clínica Las Condes , Santiago , Chile
AuthorAffiliation_xml	– name: 4 Inflammatory Bowel Diseases Program, Department of Gastroenterology, Clínica Las Condes , Santiago , Chile – name: 5 Department of Medical Microbiology, University of Groningen, University Medical Center Groningen , Groningen , Netherlands – name: 3 Program of Cell and Molecular Biology, Faculty of Medicine, Institute of Biomedical Sciences, Universidad de Chile , Santiago , Chile – name: 1 Laboratory of Innate Immunity, Program of Immunology, Institute of Biomedical Sciences, Faculty of Medicine, Universidad de Chile , Santiago , Chile – name: 2 Department of Gastroenterology and Hepatology, University of Groningen, University Medical Center Groningen , Groningen , Netherlands – name: 6 Department of Laboratory Medicine, University Medical Center Groningen, University of Groningen , Groningen , Netherlands
Author_xml	– sequence: 1 givenname: Daniela surname: Parada Venegas fullname: Parada Venegas, Daniela – sequence: 2 givenname: Marjorie K. surname: De la Fuente fullname: De la Fuente, Marjorie K. – sequence: 3 givenname: Glauben surname: Landskron fullname: Landskron, Glauben – sequence: 4 givenname: María Julieta surname: González fullname: González, María Julieta – sequence: 5 givenname: Rodrigo surname: Quera fullname: Quera, Rodrigo – sequence: 6 givenname: Gerard surname: Dijkstra fullname: Dijkstra, Gerard – sequence: 7 givenname: Hermie J. M. surname: Harmsen fullname: Harmsen, Hermie J. M. – sequence: 8 givenname: Klaas Nico surname: Faber fullname: Faber, Klaas Nico – sequence: 9 givenname: Marcela A. surname: Hermoso fullname: Hermoso, Marcela A.
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/30915065$$D View this record in MEDLINE/PubMed
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Keywords	SCFAs immune cells IBD intestinal mucosa IECs dysbiosis
Language	English
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Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 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
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Snippet	Ulcerative colitis (UC) and Crohn's disease (CD), collectively known as Inflammatory Bowel Diseases (IBD), are caused by a complex interplay between genetic,...
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SubjectTerms	dysbiosis IBD IECs immune cells Immunology intestinal mucosa SCFAs
Title	Short Chain Fatty Acids (SCFAs)-Mediated Gut Epithelial and Immune Regulation and Its Relevance for Inflammatory Bowel Diseases
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