In order to explore the effects of testicular infection of murine cytomegalovirus (MCMV) on mature sperm viability at different periods following MCMV inoculation in mice, 91 BALB/c mice without MCMV infection were randomly divided into two groups: an experimental group (n = 56) and a control group (n = 35). The mice in the experimental group were treated by inoculating MCMV intratesticularly, while those in the controlled group were directly inoculated with DMEM without MCMV. The mice in both groups were sacrificed separately on the day 1, 1. 5, 2, 4, 6, 9 and 14 post-inoculation (D1) 1. 5, 2, 4, 6, 9 and 14 PI). The MCMV M83 mRNA gene was detected in the testis by in situ hybridization (ISH) with MCMV late-mRNA probe labeled with digoxin. Sperm viability of mature sperm in the epididymis cauda was measured. The results demonstrated the positive signal of ISH of MCMV was found mainly in the cytoplasm of the testicular interstitial cells and spermatogenic cells in the experimental group. Compared with that in the controlled group, the sperm viability in the experimental group was decreased significantly on D1 PI and D1.5 PI (P < 0.05). No statistically significant difference in the sperm viability was found after D2 PI between two groups (P > 0.05). This suggested that sperm viability in mice might be descended significantly shortly after MCMV infection and might return to normal with time, indicating that MCMV acute infection might temporarily degrade sperm quality and influence procreation transiently.
Previous studies have shown that PM2.5 is associated with airway inflammation and lung injury. However, the association between traffic-related PM2.5 (TR-PM) exposure and OVA-induced allergic inflammation is not fully elucidated. In this study, we assessed allergic inflammatory responses of mice induced by TR-PM. PM2.5 was collected from a roadside with heavy traffic, and its soluble extract was prepared. Mice were treated with OVA, TR-PM alone, and OVA + TR-PM. The inflammatory cells were counted, and inflammation-related cytokines IL-4, IL-17A, and IL-10 in bronchoalveolar lavage fluid (BALF) were determined by the radioimmunity assay. Allergy-induced inflammation and lung injury were investigated by histopathological analyses. The expression of IL-4, IL-17A, and IL-10 mRNA was analyzed by RT-PCR. Our results revealed that TR-PM exposure, combined with OVA allergen sensitization, increased the inflammatory cells in BALF as well as levels of IgE in lung tissue; increased the IL-4 and IL-17A levels in BALF significantly, but decreased IL-10 level. The histopathologic results demonstrated that TR-PM markedly exacerbated the OVA-induced neutrophilic granulocyte, lymphocyte, and macrophage infiltration. Furthermore, the expression of IL-4, IL-17A and IL-10 mRNA was well in agreement with the results of the inflammatory cytokines. In conclusion, during the sensitization to allergic antigens, TR-PM exposure triggers severe allergic inflammation and lung injury. These findings suggest that commuters should use public transportation instead of riding motorcycles or walking during rush hours.
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