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

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

Research output: Contribution to journalArticle

58 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)889-900
Number of pages12
JournalImmunity
Volume44
Issue number4
DOIs
Publication statusPublished - 2016 Apr 19

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Toll-Like Receptor 7
Toll-Like Receptor 3
Enterovirus
Interferons
Colitis
Dextran Sulfate
Inflammation
Viruses
Metagenomics
Rotavirus
Ulcerative Colitis
Dendritic Cells
Antiviral Agents
Immunity
Colon
Homeostasis
Maintenance

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

Cite this

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. / Enteric Viruses Ameliorate Gut Inflammation via Toll-like Receptor 3 and Toll-like Receptor 7-Mediated Interferon-β Production. In: Immunity. 2016 ; Vol. 44, No. 4. pp. 889-900.
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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.",
author = "Yang, {Jin Young} and Kim, {Min Soo} and Eugene Kim and Cheon, {Jae Hee} and Lee, {Yong Soo} and Yeji Kim and Lee, {Su Hyun} and Seo, {Sang Uk} and Shin, {Seung Ho} and Choi, {Sun Shim} and Bumseok Kim and Chang, {Sun Young} and Ko, {Hyun Jeong} and Bae, {Jin Woo} and Kweon, {Mi Na}",
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Yang, JY, Kim, MS, Kim, E, Cheon, JH, Lee, YS, Kim, Y, Lee, SH, Seo, SU, Shin, SH, Choi, SS, Kim, B, Chang, SY, Ko, HJ, Bae, JW & Kweon, MN 2016, 'Enteric Viruses Ameliorate Gut Inflammation via Toll-like Receptor 3 and Toll-like Receptor 7-Mediated Interferon-β Production', Immunity, vol. 44, no. 4, pp. 889-900. https://doi.org/10.1016/j.immuni.2016.03.009

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

In: Immunity, Vol. 44, No. 4, 19.04.2016, p. 889-900.

Research output: Contribution to journalArticle

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AU - Cheon, Jae Hee

AU - Lee, Yong Soo

AU - Kim, Yeji

AU - Lee, Su Hyun

AU - Seo, Sang Uk

AU - Shin, Seung Ho

AU - Choi, Sun Shim

AU - Kim, Bumseok

AU - Chang, Sun Young

AU - Ko, Hyun Jeong

AU - Bae, Jin Woo

AU - Kweon, Mi Na

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N2 - 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.

AB - 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.

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