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P40: Uterine colonization with Mobiluncus mulieris is insufficient to cause preterm birth

Method of Study: 8-10-week-old male B6 mice were used for the induction of the EAEO model. EAEO mice were administrated with 10% glucose and the controls were treated by regular water drinking. On day 90 post EAEO induction, the histopathological evaluation was performed by HE and Masson staining from the testis and epididymis sections. Mouse sperm apoptosis, ROS generation of draining lymph nodes, and the immunophenotyping of T cell subsets in draining lymph nodes, testis, and epididymis, were evaluated via Flowcytometry. Results: HE and Masson staining of histological features showed the impaired spermatogenesis impairment aggravated with germ cell loss in testis, fibrotic remodeling, and collagen deposition in epididymis from mice received 10% glucose supplement. Reduced sperm counts and viability with higher lever ROS could be detected in cauda epididymis sperm from EAEO mice with 10% glucose intake compared with the control group. Compared to the usual drinking group on, a higher th17 (T helper 17) cells proportion and cell numbers of the day 90 after EAEO induction was maintained in both epididymis and testis of those with 10% glucose fed. The pathogenic Th17 (CCR6+IL17a+)cells are the central source of mitochondrial ROS in the draining lymph nodes CD4+T cells. Conclusions: we demonstrated that high-level glucose intake exacerbated autoimmunity in EAEO models by promoting Th17 cell differentiation. We further elucidated that high glucose drived the differentiation of the th17 cells, followed by the increased generation of mitochondrial ROS in the pathogenic Th17 (CCR6+IL-17a+) cells and poor sperm parameters outcome. Moreover, these findings uncovered a potential mechanism underlying the adverse consequences of high-level glucose intake during male fertility impairment and autoimmunity development, which may have clinical implications.