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Enteric Viruses Ameliorate Gut Inflammation via Toll-like Receptor 3 and Toll-like Receptor 7-Mediated Interferon-β Production

Immunity (Cambridge, Mass.), 2016-04, Vol.44 (4), p.889-900 [Peer Reviewed Journal]

2016 Elsevier Inc. ;Copyright © 2016 Elsevier Inc. All rights reserved. ;ISSN: 1074-7613 ;EISSN: 1097-4180 ;DOI: 10.1016/j.immuni.2016.03.009 ;PMID: 27084119

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Title:
Enteric Viruses Ameliorate Gut Inflammation via Toll-like Receptor 3 and Toll-like Receptor 7-Mediated Interferon-β Production
Author: Yang, Jin-Young ; Kim, Min-Soo ; Kim, Eugene ; Cheon, Jae Hee ; Lee, Yong-Soo ; Kim, Yeji ; Lee, Su-Hyun ; Seo, Sang-Uk ; Shin, Seung-Ho ; Choi, Sun Shim ; Kim, Bumseok ; Chang, Sun-Young ; Ko, Hyun-Jeong ; Bae, Jin-Woo ; Kweon, Mi-Na
Subjects: Animals ; Antiviral Agents - pharmacology ; Colitis - chemically induced ; Colitis - immunology ; Dendritic Cells - immunology ; Dextran Sulfate ; Gastrointestinal Microbiome ; Gastrointestinal Tract - immunology ; Gastrointestinal Tract - virology ; Humans ; Inflammation - immunology ; Interferon-beta - biosynthesis ; Interferon-beta - immunology ; Membrane Glycoproteins - genetics ; Membrane Glycoproteins - immunology ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; RNA, Ribosomal, 16S - genetics ; Rotavirus - immunology ; Toll-Like Receptor 3 - genetics ; Toll-Like Receptor 3 - immunology ; Toll-Like Receptor 7 - genetics ; Toll-Like Receptor 7 - immunology
Is Part Of: Immunity (Cambridge, Mass.), 2016-04, Vol.44 (4), p.889-900
Description: Metagenomic studies show that diverse resident viruses inhabit the healthy gut; however, little is known about the role of these viruses in the maintenance of gut homeostasis. We found that mice treated with antiviral cocktail displayed more severe dextran sulfate sodium (DSS)-induced colitis compared with untreated mice. DSS-induced colitis was associated with altered enteric viral abundance and composition. When wild-type mice were reconstituted with Toll-like receptor 3 (TLR3) or TLR7 agonists or inactivated rotavirus, colitis symptoms were significantly ameliorated. Mice deficient in both TLR3 and TLR7 were more susceptible to DSS-induced experimental colitis. In humans, combined TLR3 and TLR7 genetic variations significantly influenced the severity of ulcerative colitis. Plasmacytoid dendritic cells isolated from inflamed mouse colon produced interferon-β in a TLR3 and TLR7-dependent manner. These results imply that recognition of resident viruses by TLR3 and TLR7 is required for protective immunity during gut inflammation. [Display omitted] •Pre-treatment with an antiviral cocktail results in severe colitis•Treatment with TLR3+7 agonists and inactivated rotavirus ameliorates colitis•Tlr3−/−Tlr7−/− mice are more susceptible to colitis•TLR3+7 agonists stimulate IFN-β secretion by pDCs from inflamed colon The role of gut resident viruses in the maintenance of homeostasis is unclear. Kweon and colleagues show the sensing of gut viruses by TLR3 or TLR7 enhances the production of interferon-β that dampens inflammation.
Publisher: United States: Elsevier Inc
Language: English
Identifier: ISSN: 1074-7613
EISSN: 1097-4180
DOI: 10.1016/j.immuni.2016.03.009
PMID: 27084119
Source: Cell Press Free Archives
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Enteric Viruses Ameliorate Gut Inflammation via Toll-like Receptor 3 and Toll-like Receptor 7-Mediated Interferon-β Production

2016 Elsevier Inc. ;Copyright © 2016 Elsevier Inc. All rights reserved. ;ISSN: 1074-7613 ;EISSN: 1097-4180 ;DOI: 10.1016/j.immuni.2016.03.009 ;PMID: 27084119

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