Mumps virus-induced innate immune responses in mouse Sertoli and Leydig cells

Mumps virus (MuV) infection frequently causes orchitis and impairs male fertility. However, the mechanisms underlying the innate immune responses to MuV infection in the testis have yet to be investigated. This study showed that MuV induced innate immune responses in mouse Sertoli and Leydig cells t...

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Bibliographic Details
Published in:Scientific reports 2016-01, Vol.6 (1), p.19507-19507, Article 19507
Main Authors: Wu, Han, Shi, Lili, Wang, Qing, Cheng, Lijing, Zhao, Xiang, Chen, Qiaoyuan, Jiang, Qian, Feng, Min, Li, Qihan, Han, Daishu
Format: Article
Language:English
Subjects:
Adaptor Proteins, Signal Transducing - metabolism
Animals
Chemokines
Cytokines
Cytokines - genetics
Cytokines - metabolism
Disease Models, Animal
Fertility
Gene Expression Regulation
Immune response
Immunity, Innate
Immunology
Infections
Innate immunity
Interferon Regulatory Factor-3 - metabolism
Leydig Cells - immunology
Leydig Cells - metabolism
Leydig Cells - virology
Male
Membrane Proteins - metabolism
Mice
Mice, Knockout
Mumps - genetics
Mumps - immunology
Mumps - metabolism
Mumps - virology
Mumps virus - immunology
Nerve Tissue Proteins - metabolism
NF-kappa B - metabolism
Rodents
Sertoli Cells - immunology
Sertoli Cells - metabolism
Sertoli Cells - virology
Testosterone - biosynthesis
Toll-Like Receptor 2 - genetics
Toll-Like Receptor 2 - metabolism
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Summary:Mumps virus (MuV) infection frequently causes orchitis and impairs male fertility. However, the mechanisms underlying the innate immune responses to MuV infection in the testis have yet to be investigated. This study showed that MuV induced innate immune responses in mouse Sertoli and Leydig cells through TLR2 and retinoic acid-inducible gene I (RIG-I) signaling, which result in the production of proinflammatory cytokines and chemokines, including TNF-α, IL-6, MCP-1, CXCL10, and type 1 interferons (IFN-α and IFN-β). By contrast, MuV did not induce the cytokine production in male germ cells. In response to MuV infection, Sertoli cells produced higher levels of proinflammatory cytokines and chemokines but lower levels of type 1 IFNs than Leydig cells did. The MuV-induced cytokine production by Sertoli and Leydig cells was significantly reduced by the knockout of TLR2 or the knockdown of RIG-I signaling. The local injection of MuV into the testis triggered the testicular innate immune responses in vivo. Moreover, MuV infection suppressed testosterone synthesis by Leydig cells. This is the first study examining the innate immune responses to MuV infection in testicular cells. The results provide novel insights into the mechanisms underlying the MuV-induced innate immune responses in the testis.
ISSN:2045-2322
2045-2322
DOI:10.1038/srep19507