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

Authors
 Jin-Young Yang  ;  Min-Soo Kim  ;  Eugene Kim  ;  Jae Hee Cheon  ;  Yong-Soo Lee  ;  Yeji Kim  ;  Su-Hyun Lee  ;  Sang-Uk Seo  ;  Seung-Ho Shin  ;  Sun Shim Choi  ;  Bumseok Kim  ;  Sun-Young Chang  ;  Hyun-Jeong Ko  ;  Jin-Woo Bae  ;  Mi-Na Kweon 
Citation
 IMMUNITY, Vol.44(4) : 889-900, 2016 
Journal Title
IMMUNITY
ISSN
 1074-7613 
Issue Date
2016
MeSH
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*
Abstract
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.
Full Text
http://www.sciencedirect.com/science/article/pii/S107476131630098X
DOI
10.1016/j.immuni.2016.03.009
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Cheon, Jae Hee(천재희) ORCID logo https://orcid.org/0000-0002-2282-8904
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/147064
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