Centre for Reproduction and Development, Monash Institute of Medical Research, Monash University, 27-31 Wright Street, Clayton, Melbourne, Victoria 3168, Australia.
J Reprod Immunol. 2011 Mar;88(2):130-41. doi: 10.1016/j.jri.2011.01.010. Epub 2011 Feb 18.
It is self-evident that infection and inflammation in the reproductive tract can inhibit male fertility, but the observation that fertility may also be compromised by systemic inflammation and disease is more difficult to explain. Recent studies implicating microbial pattern-recognition receptors, such as the Toll-like receptors (TLRs), as well as inflammatory cytokines and their signalling pathways, in testicular function have cast new light on this mysterious link between infection/inflammation and testicular dysfunction. It is increasingly evident that signalling pathways normally involved in controlling inflammation play fundamental roles in regulating Sertoli cell activity and responses to reproductive hormones, in addition to promoting immune responses within the testis. Many of the negative effects of inflammation on spermatogenesis may be attributed to elevated production of inflammation-related gene products within the circulation and the testis, which subsequently exert disruptive effects on spermatogenic cell development and survival, as well as the ability of the Sertoli cells to provide support for spermatogenesis. These interactions have important implications for testicular dysfunction and disease, and may eventually provide new opportunities for therapeutic interventions.
生殖道感染和炎症显然会抑制男性生育力，但观察到全身炎症和疾病也可能会损害生育力，这更难解释。最近的研究表明，微生物模式识别受体（如 Toll 样受体（TLRs））以及炎症细胞因子及其信号通路在睾丸功能中起作用，这为感染/炎症与睾丸功能障碍之间的神秘联系提供了新的线索。越来越明显的是，正常参与控制炎症的信号通路在调节支持细胞的活性和对生殖激素的反应方面发挥着重要作用，除了促进睾丸内的免疫反应之外。炎症对精子发生的许多负面影响可能归因于循环和睾丸中炎症相关基因产物的产生增加，这随后对精子发生细胞的发育和存活以及支持细胞提供支持精子发生的能力产生破坏性影响。这些相互作用对睾丸功能障碍和疾病具有重要意义，并可能最终为治疗干预提供新的机会。
