Department of Oral Biology and Biomedical Sciences, Faculty of Dentistry, MAHSA University, Kuala Lumpur, Malaysia.
Department of Physiology, Faculty of Medicine, Bioscience and Nursing, MAHSA University, Kuala Lumpur, Malaysia.
Mol Cell Biochem. 2020 Nov;474(1-2):57-72. doi: 10.1007/s11010-020-03833-4. Epub 2020 Jul 20.
Infertility is a subject of worldwide concern as it affects approximately 15% of couples. Among the prime contributors of infertility, urogenital bacterial infections have lately gained much clinical importance. Staphylococcal species are commensal bacteria and major human pathogens mediating an array of reproductive tract infections. Emerging evidences are 'bit by bit' revealing the mechanisms by which Staphylococci strategically disrupt normal reproductive functions. Staphylococcal species can directly or through hematogenous routes can invade the reproductive tissues. In the testicular cells, epididymis as well as in various compartments of female reproductive tracts, the pathogen recognition receptors, toll-like receptors (TLRs), can recognize the pathogen-associated molecular patterns on the Staphylococci and thereby activate inflammatory signalling pathways. These elicit pro-inflammatory mediators trigger other immune cells to infiltrate and release further inflammatory agents and reactive oxygen species (ROS). Adaptive immune responses may intensify the inflammation-induced reproductive tissue damage, particularly via activation of T-helper (Th) cells, Th1 and Th17 by the innate components or by staphylococcal exotoxins. Staphylococcal surface factors binding with sperm membrane proteins can directly impair sperm functions. Although Staphylococci, being one of the most virulent bacterial species, are major contributors in infection-induced infertility in both males and females, the mechanisms of their operations remain under-discussed. The present review aims to provide a comprehensive perception of the possible mechanisms of staphylococcal infection-induced male and female infertility and aid potential interventions to address the lack of competent therapeutic measures for staphylococcal infection-induced infertility.
不孕不育是一个全球性关注的问题，因为它影响了大约 15%的夫妇。在导致不孕不育的主要因素中，泌尿生殖系统细菌感染最近引起了更多的临床关注。葡萄球菌是共生菌，也是介导一系列生殖道感染的主要人类病原体。新出现的证据“一点一滴”地揭示了葡萄球菌策略性地破坏正常生殖功能的机制。葡萄球菌可以通过直接或血源性途径侵犯生殖组织。在睾丸细胞、附睾以及女性生殖道的各个部位，病原体识别受体，即 Toll 样受体 (TLR)，可以识别葡萄球菌上的病原体相关分子模式，从而激活炎症信号通路。这些促炎介质引发其他免疫细胞浸润并释放进一步的炎症介质和活性氧 (ROS)。适应性免疫反应可能会加剧炎症引起的生殖组织损伤，特别是通过先天成分或葡萄球菌外毒素激活辅助性 T 细胞 (Th)、Th1 和 Th17。葡萄球菌表面因子与精子膜蛋白结合可以直接损害精子功能。尽管葡萄球菌是最具毒性的细菌之一，是男性和女性感染性不孕的主要原因之一，但它们的作用机制仍未得到充分讨论。本综述旨在全面了解葡萄球菌感染引起的男性和女性不孕的可能机制，并为解决葡萄球菌感染引起的不孕缺乏有效治疗措施提供潜在干预措施。
