病菌感染对男性生育力和精子授精能力的影响
About 7 percent of all men are confronted with fertility problems during their reproductive lifetime, which has an even higher prevalence than a common disease. Causes for male infertility can be different and apart from idiopathic infertility (28.4%) and varicocele (18.1%), male genital tract infections are the third single most (11.6%) cause of male infertility (1).
大约7%的育龄男性会面临生育困难，其患病率甚至高于常见疾病。造成男性不育的原因可能有很多种，除了原发性不育(28.4%)和精索静脉曲张(18.1%)外，生殖道感染是男性不育的第三大原因(11.6%)(1)。
Depending on the site, infections and inflammations can seriously affect spermatogenesis and sperm transit during ejaculation as can be seen in clinical findings in cases of oligozoospermia, asthenozoospermina and azoospermia (2). Chronic infections of the male genital tract including the accessory glands are often scarring and result in obstruction (3). Moreover, they can cause dysfunctional male accessory glands and significantly impair sperm functions (4). These changes are triggered by direct action of the pathogens on spermatozoa and sperm functions or indirectly by inducing inflammatory processes in the seminal tract by activating leukocytes (5).
感染和炎症根据其发生部位可能会严重影响生精能力和射精过程中的精子传输，与少精症，弱精症和无精症的临床表现相符(2)。 男性生殖道例如附属腺体发生慢性感染时，通常会导致腺体瘢痕化而引起阻塞(3)。此外，它们还会导致男性附属腺体功能障碍，严重损害精子功能(4)，这些都是由病原体对精子和精子功能的直接作用或者是在精道中激活白细胞产生炎症反应引起的。
Sperm fertilizing capacity may directly be compromised by activated leukocytes infiltrating the infected organs and releasing high amounts of reactive oxygen species (ROS) and cytokines such as IL-6, IL-8 or TNF-α as inflammatory mediators (6). Both, ROS and cytokins have been shown to be associated with the impairment of various sperm functions including the sperm DNA through oxidative stress (7). The mechanism by which this damage takes place involves oxidation of sperm membranes by means of lipid peroxidation as well as direct oxidation of the DNA (8).
活化的白细胞浸润受感染器官并释放大量活性氧和细胞因子例如IL-6，IL-8和TNF-α来充当炎症介质，并因此直接损害精子授精能力。活性氧和细胞因子均已被证明与各种精子功能受损有关，包括通过氧化应激反应损坏精子DNA(7)。这种损伤发生机制包括通过脂质过氧作用氧化精子膜以及对精子DNA的直接氧化作用(8)。
Clinical reports indicate that infections and chronic inflammation may even impair testicular steroidogenesis and spermatogenesis resulting in temporary or permanent infertility (9). In animal experiments, local production of IL-1β and TNF-α has been reported to be responsible for a down-regulation of cholesterol transport protein, steroidogenic acute regulatory protein (StAR) and various enzymes of the steroid synthesis pathway (10).
临床报告显示，感染和慢性炎症甚至可能阻碍睾丸类固醇生成和精子生成，导致暂时或永久性不育(9)。在动物实验中发现，自体生成的IL-1β and TNF-α是导致胆固醇转运蛋白，类固醇合成急性调节蛋白(StAR)和类固醇合成途径的各种酶生成下降的原因(10)。
Furthermore, significant production of proinflammatory cytokines also activate the hypothalamic-pituitary-adrenal axis leading to an increased secretion of glucocorticoids, which, in turn, inhibit steroidogenesis via the hypothalamus and pituitary (11). Thus, an infection mediated via lipopolysaccharides may inhibit Leydig cell function resulting in reduced testosterone synthesis as shown in an animal model (12).
此外，炎症细胞因子的大量产生也会激活下丘脑-垂体-肾上腺轴分泌更多糖皮质激素，糖皮素激素的增加会反过来抑制下丘脑和垂体生成类固醇(11)。因此，正如动物实验结果所示，通过脂多糖介导的感染可能会抑制莱迪希细胞功能，导致睾酮合成减少(12)。
References
参考文献
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