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).
大約7%的育齡男性會(huì)面臨生育困難，其患病率甚至高于常見(jiàn)疾病。造成男性不育的原因可能有很多種，除了原發(fā)性不育(28.4%)和精索靜脈曲張(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).
感染和炎癥根據(jù)其發(fā)生部位可能會(huì)嚴(yán)重影響生精能力和射精過(guò)程中的精子傳輸，與少精癥，弱精癥和無(wú)精癥的臨床表現(xiàn)相符(2)。 男性生殖道例如附屬腺體發(fā)生慢感染性
時(shí)，通常會(huì)導(dǎo)致腺體瘢痕化而引起阻塞(3)。此外，它們還會(huì)導(dǎo)致男性附屬腺體功能障礙，嚴(yán)重?fù)p害精子功能(4)，這些都是由病原體對(duì)精子和精子功能的直接作用或者是在精道中激活白細(xì)胞產(chǎn)生炎癥反應(yīng)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).
活化的白細(xì)胞浸潤(rùn)受感染器官并釋放大量活性氧和細(xì)胞因子例如IL-6，IL-8和TNF-α來(lái)充當(dāng)炎癥介質(zhì)，并因此直接損害精子授精能力。活性氧和細(xì)胞因子均已被證明與各種精子功能受損有關(guān)，包括通過(guò)氧化應(yīng)激反應(yīng)損壞精子DNA(7)。這種損傷發(fā)生機(jī)制包括通過(guò)脂質(zhì)過(guò)氧作用氧化精子膜以及對(duì)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).
臨床報(bào)告顯示，感染和慢性炎癥甚至可能阻礙睪丸類(lèi)固醇生成和精子生成，導(dǎo)致暫時(shí)或長(zhǎng)久性不育(9)。在動(dòng)物實(shí)驗(yàn)中發(fā)現(xiàn)，自體生成的IL-1β and TNF-α是導(dǎo)致膽固醇轉(zhuǎn)運(yùn)蛋白，類(lèi)固醇合成急性調(diào)節(jié)蛋白(StAR)和類(lèi)固醇合成途徑的各種酶生成下降的原因(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，炎癥細(xì)胞因子的大量產(chǎn)生也會(huì)激活下丘腦-垂體-腎上腺軸分泌更多糖皮質(zhì)激素，糖皮素激素的增加會(huì)反過(guò)來(lái)控制下丘腦和垂體生成類(lèi)固醇(11)。因此，正如動(dòng)物實(shí)驗(yàn)結(jié)果所示，通過(guò)脂多糖介導(dǎo)的感染可能會(huì)控制萊迪希細(xì)胞功能，導(dǎo)致睪酮合成減少(12)。
Refences
參考文獻(xiàn)
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