不育原因探秘：成都男性生殖道感染如何影响精子质量？

　　About 7 pcent of all men are confronted with ftility problems during their reproductive lifetime, which has an even high prevalence than a common disease. Causes for male inftility can be diffent and apart from idiopathic inftility (28.4%) and varicocele (18.1%), male genital tract infections are the third single most (11.6%) cause of male inftility (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 sious affect spmatogenesis and spm transit during ejaculation as can be seen in clinical findings in cases of oligozoospmia, asthenozoospmina and azoospmia (2). Chronic infections of the male genital tract including the accessory glands are often scarring and result in obstruction (3). Moreov, they can cause sfunctional male accessory glands and significant impair spm functions (4). These changes are trigged by direct action of the pathogens on spmatozoa and spm functions or indirect 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感染性时，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。

　　Spm ftilizing capacity may direct be compromised by activated leukocytes infiltrating the infected organs and releasing high amounts of reactive o.gen 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 spm functions including the spm DNA through oxidative stress (7). The mechanism by which this damage takes place iolves oxidation of spm membranes by means of lipid poxidation 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 stoidogenesis and spmatogenesis resulting in temporary or pmanent inftility (9). In animal expiments, local production of IL-1β and TNF-α has been reported to be responsible for a down-regulation of chotol transport protein, stoidogenic acute regulatory protein (StAR) and various enzymes of the stoid 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，导致暂时或长久性不育(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)。

　　Furthmore, significant production of proinflammatory cytokines also activate the hypothalamic-pituitary-adrenal axis leading to an increased secretion of glucocorticoids, which, in turn, inhibit stoidogenesis via the hypothalamus and pituitary (11). Thus, an infection mediated via lipoposaccharides may inhibit Leydig cell function resulting in reduced testostone 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控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控制莱迪希细胞功能，导致睾酮合成减少(12)。

　　Refences

　　参考文献

　　1. Nieschlag E, Behre H. Andrology. Male Reproductive Health and Dysfunction 1997; Spring, Blin.

　　2. Weidn W, Colpi GM, Hargreave TB, et al. EAU guidelines on male inftility. Eur Uro 2002;42:313-22.

　　3. Goluboff ET, Stifelman MD, Fisch H. Ejaculatory duct obstruction in the inftile male. Urology 1995;45:925-31.

　　4. Henkel R, Schill W-B. Spm separation in patients with urogenital infections. Andrologia 1998;30 (Suppl. 1):91-7.

　　5. Eggt-Kruse W, Kief I, Beck C, et al. Role for tumor necrosis factor alpha (TNF-alpha) and intleukin 1-beta (IL-1beta) detmination in seminal plasma during inftility iestigation. Ftil Stil 2007;87:810-23.

　　6. Comhaire F, Mahmoud A. Infection/inflammation of the accessory sex glands. In: Schill W-B, Comhaire F, Hargreave TB (Eds). Andrology for the Clinician 2006; Spring, Heidelbg, pp.72-74.

　　7. Henkel R, Hajimohanmad M, Stalf T, et al. Influence of deo.ribonucleic acid damage on ftilization and pregcy. Ftil Stil 2004;81:965-72.

　　8. Martinez R, Provbio F, Camejo MI. Spm lipid poxidation and pro-inflammatory cytokines. Asian J Androl 2007;9:102-7.

　　9. Bak HW. Reproductive effects of nontesticular illness. Endocrinol Metab Clin North Am 1998;27:831-850.

　　10. Ha DB, Xiong Y, Tur-Kaspa I. The role of cytokines in the regulation of Leydig cell P450c17 gene expression. J Stoid Biochem 1992;43:907-14.

　　11. Bombino TH, HAJ. Direct inhibitory effect of glucocorticoids upon testicular luteinizing hormone receptor and stoidogenesis in vivo and in vitro. Endocrinology 1981;108:2142-8.

　　12. Gow RM, O’Bryan MK, Canny BJ, et al. Diffential effects of dexamethasone treatment on lipoposaccharide-induced testicular inflammation and reproductive hormone inhibition in adult rats. J Endocrinol 2001;168:193-201.