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Updated: Aug 12, 2026
Mouse Models of Epididymitis Induced by Pathogen-Associated Molecular Patterns
Published on: December 12, 2025
Mumps Virus-Induced TNF-α Production Through Toll-Like Receptor 2 Mediates Testicular Dysfunction in Male Mice
Lili Shi1, Fei Wang1, Qian Jiang1
1Institute of Basic Medical Sciences & School of Basic Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Abstract:
Mumps virus (MuV) infection may lead to male infertility. However, the pathological mechanisms of testicular dysfunctions are largely unknown. This study aims to the mechanisms by which MuV infection induces testicular dysfunctions in mice. Intraperitoneal injection of MuV induced up-regulation of cytokines and chemokines including tumor necrosis factor alpha (TNF-α), monocyte tractant-1, IP-10. Moreover, MuV infection induced male germ cell apoptosis and impaired spermatogenesis. Notably, MuV injection did not evidently induce dysfunction in Toll-like receptor 2 knockout (TLR2-/-) or TNF-α-/- mice. MuV did not induce TNF-α production in TLR2-/- mice. The results suggest that MuV induces TNF-α production through TLR2, and TNF-α leads to testicular dysfunction. Data of this study provide novel insights into the mechanisms underlying MuV-induced testicular dysfunction in mice.
Insights
Mumps virus (MuV) causes male infertility by triggering inflammatory cytokines like tumor necrosis factor alpha (TNF-α) via Toll-like receptor 2 (TLR2). This leads to germ cell death and impaired sperm production.
Area of Science:
- Immunology
- Reproductive Biology
- Virology
Background:
- Mumps virus (MuV) infection is linked to male infertility, but the underlying pathological mechanisms remain unclear.
- Understanding how MuV affects testicular function is crucial for developing targeted therapies.
Purpose of the Study:
- To elucidate the mechanisms by which MuV infection induces testicular dysfunction in a mouse model.
- To investigate the role of specific cytokines and receptors in MuV-induced testicular damage.
Main Methods:
- Mice were intraperitoneally injected with MuV.
- Cytokine and chemokine levels (TNF-α, MCP-1, IP-10) were measured.
- Germ cell apoptosis and spermatogenesis were assessed.
- Experiments were conducted using Toll-like receptor 2 knockout (TLR2-/-) and TNF-α knockout (TNF-α-/-) mice.
Main Results:
- MuV infection upregulated pro-inflammatory cytokines and chemokines, including tumor necrosis factor alpha (TNF-α).
- MuV induced male germ cell apoptosis and impaired spermatogenesis.
- Testicular dysfunction was not evident in TLR2-/- or TNF-α-/- mice, and MuV did not induce TNF-α production in TLR2-/- mice.
Conclusions:
- MuV induces TNF-α production through TLR2 activation.
- TNF-α plays a critical role in mediating MuV-induced testicular dysfunction.
- These findings offer new insights into the pathogenesis of mumps virus-related male infertility.
