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PMID: 25731162 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome.

Nature ·Vol. 519 ·No. 7541 ·2015-00-05 ·Pages 92-6

Chassaing B, Koren O, Goodrich JK, Poole AC, Srinivasan S, Ley RE, Gewirtz AT

Abstract

The intestinal tract is inhabited by a large and diverse community of microbes collectively referred to as the gut microbiota. While the gut microbiota provides important benefits to its host, especially in metabolism and immune development, disturbance of the microbiota-host relationship is associated with numerous chronic inflammatory diseases, including inflammatory bowel disease and the group of obesity-associated diseases collectively referred to as metabolic syndrome. A primary means by which the intestine is protected from its microbiota is via multi-layered mucus structures that cover the intestinal surface, thereby allowing the vast majority of gut bacteria to be kept at a safe distance from epithelial cells that line the intestine. Thus, agents that disrupt mucus-bacterial interactions might have the potential to promote diseases associated with gut inflammation. Consequently, it has been hypothesized that emulsifiers, detergent-like molecules that are a ubiquitous component of processed foods and that can increase bacterial translocation across epithelia in vitro, might be promoting the increase in inflammatory bowel disease observed since the mid-twentieth century. Here we report that, in mice, relatively low concentrations of two commonly used emulsifiers, namely carboxymethylcellulose and polysorbate-80, induced low-grade inflammation and obesity/metabolic syndrome in wild-type hosts and promoted robust colitis in mice predisposed to this disorder. Emulsifier-induced metabolic syndrome was associated with microbiota encroachment, altered species composition and increased pro-inflammatory potential. Use of germ-free mice and faecal transplants indicated that such changes in microbiota were necessary and sufficient for both low-grade inflammation and metabolic syndrome. These results support the emerging concept that perturbed host-microbiota interactions resulting in low-grade inflammation can promote adiposity and its associated metabolic effects. Moreover, they suggest that the broad use of emulsifying agents might be contributing to an increased societal incidence of obesity/metabolic syndrome and other chronic inflammatory diseases.

MeSH Terms
Adiposity/drug effects Animals Carboxymethylcellulose Sodium/administration & dosage,adverse effects Colitis/chemically induced,microbiology,pathology Diet/adverse effects Emulsifying Agents/administration & dosage,adverse effects Feces/microbiology Female Gastrointestinal Tract/drug effects,microbiology,pathology Germ-Free Life Inflammation/chemically induced,microbiology,pathology Intestinal Mucosa/drug effects,microbiology,pathology Male Metabolic Syndrome/chemically induced,microbiology,pathology Mice Microbiota/drug effects Obesity/chemically induced,microbiology,pathology Polysorbates/administration & dosage,adverse effects
Chemicals
Emulsifying Agents Polysorbates Carboxymethylcellulose Sodium
Authors & Affiliations
7 authors, click to expand affiliations / ORCID
Chassaing Benoit
Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia 30303, USA.
Koren Omry
Faculty of Medicine, Bar Ilan University, Safed, 13115, Israel.
Goodrich Julia K
Department of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853, USA.
Poole Angela C
Department of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853, USA.
Srinivasan Shanthi
Digestive Diseases Division, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
Ley Ruth E
Department of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853, USA.
Gewirtz Andrew T
Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, Georgia 30303, USA.
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Article Info
Journal
Nature
Abbr.
Nature
ISSN
1476-4687
Published
2015-00-05
Epub
2015-00-25
Pages
92-6
Language
English
Region
England
NLM ID
0410462
PMCID
PMC4910713
Subset
IM
Grants
NIDDK NIH HHS · R01 DK099071 · United States
NIDDK NIH HHS · DK083890 · United States
NIDDK NIH HHS · R01 DK083890 · United States
NIDDK NIH HHS · DK099071 · United States
NIDDK NIH HHS · U24 DK097153 · United States
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