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Immunity. 2016 Apr 19;44(4):889-900. doi: 10.1016/j.immuni.2016.03.009. Epub 2016 Apr 12.

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

Author information

1
Mucosal Immunology Laboratory, Department of Convergence Medicine, University of Ulsan College of Medicine/Asan Medical Center, Seoul 05505, Korea.
2
Department of Life and Nanopharmaceutical Sciences and Department of Biology, Kyung Hee University, Seoul 02447, Korea.
3
Department of Internal Medicine and Institute of Gastroenterology, Yonsei University College of Medicine, Seoul 03722l, Korea.
4
Department of Medicine, Wide River Institute of Immunology, Seoul National University College of Medicine, Seoul 03080, Korea.
5
Department of Medical Biotechnology, College of Biomedical Science, Kangwon National University, Chuncheon 24341, Korea.
6
Laboratory of Pathology (BK21 Plus Program), College of Veterinary Medicine, Chonbuk National University, Iksan 54596, Korea.
7
Laboratory of Microbiology, College of Pharmacy, Ajou University, Suwon 16499, Korea.
8
Laboratory of Microbiology and Immunology, College of Pharmacy, Kangwon National University, Chuncheon 24341, Korea.
9
Department of Life and Nanopharmaceutical Sciences and Department of Biology, Kyung Hee University, Seoul 02447, Korea. Electronic address: baejw@khu.ac.kr.
10
Mucosal Immunology Laboratory, Department of Convergence Medicine, University of Ulsan College of Medicine/Asan Medical Center, Seoul 05505, Korea. Electronic address: mnkweon@amc.seoul.kr.

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.

PMID:
27084119
DOI:
10.1016/j.immuni.2016.03.009
[Indexed for MEDLINE]
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