Salmonella Infection Induces Orchitis and Disrupts the Blood-Testis Barrier, Leading to Spermatogenic Disorders in Mice.

This study investigated the pathological processes by which two Salmonella strains induce orchitis and impair spermatogenesis in mice, with emphasis on inflammation and blood-testis barrier (BTB) integrity. Thirty male Kunming mice were randomly assigned to the human-derived Salmonella enterica serovar Enteritidis H71 group, the sheep-derived Salmonella enterica serovar Agona W42 group, or the phosphate-buffered saline control group (n = 10 per group). An acute orchitis model was established by intrascrotal injection. Histopathological examination revealed marked testicular and epididymal lesions, disruption of the spermatogenic epithelium, and reduced sperm abundance in infected mice. Transcriptomic analysis identified 4546 differentially expressed genes shared by the two infected groups and showed enrichment of the Toll-like receptor (TLR), nuclear factor kappa B (NF-κB), and mitogen-activated protein kinase (MAPK) signaling pathways. Real-time quantitative PCR further showed increased expression of interleukin 6 (Il6), interleukin 1 beta (Il1b), and tumor necrosis factor (Tnf), accompanied by reduced expression of tight junction protein 1 (Tjp1), occludin (Ocln), and synaptonemal complex protein 3 (Sycp3) in infected mice (p < 0.05), except for Tjp1 in the W42 group. These findings indicate that Salmonella-induced inflammatory activation is associated with BTB disruption and impaired spermatogenesis, providing a basis for further investigation of bacterial orchitis and zoonotic reproductive risks.