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MyD88 Signaling in Sertoli Cells Mediates LPS-Induced Orchitis in Mice
Yuchuan Luo1, Chang Yan1, Jing Wang1
1State Key Laboratory of Animal Nutrition and Feeding, China Agricultural University, 2 Yuanmingyuan West Road, Haidian, Beijing, 100193, P.R. China.
Reproductive Sciences (Thousand Oaks, Calif.)
|August 13, 2025
Summary
Sertoli cell Myeloid differentiation primary response protein 88 (MyD88) drives inflammation in orchitis. Blocking MyD88 in Sertoli cells reduces testicular damage and improves sperm health, revealing MyD88 as a therapeutic target for male infertility.
Area of Science:
- Reproductive immunology
- Molecular biology
- Pathology
Background:
- Orchitis impairs male fertility by affecting testicular function.
- Sertoli cells regulate testicular immune responses and blood-testis barrier (BTB) integrity.
- The role of Myeloid differentiation primary response protein 88 (MyD88) in Sertoli cells during orchitis is unclear.
Purpose of the Study:
- To investigate the cell-specific role of MyD88 in Sertoli cells during lipopolysaccharide (LPS)-induced orchitis.
- To determine if MyD88 in Sertoli cells contributes to testicular inflammation and impaired fertility.
Main Methods:
- Established a murine model of LPS-induced orchitis.
- Generated Sertoli cell-specific Myd88 conditional knockout (cKO) mice.
- Assessed testicular inflammation, sperm parameters, cytokine levels, and BTB integrity.
Main Results:
- LPS challenge increased testicular MyD88 expression and inflammation.
- Sertoli cell-specific Myd88 deletion attenuated testicular edema, reduced pro-inflammatory cytokines (TNF-α, IL-6), and preserved sperm quality.
- Myd88 deletion in Sertoli cells maintained BTB integrity by restoring key component expression and mitigated neutrophil infiltration.
Conclusions:
- Sertoli cell MyD88 is a critical mediator of testicular inflammation and pathogenesis in LPS-induced orchitis.
- Targeting Sertoli cell MyD88 offers a potential therapeutic strategy for treating orchitis and preserving male fertility.
