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首页> 外文期刊>Parasitology >Antioxidant gene expression and function in in vitro-developing Schistosoma mansoni mother sporocysts: possible role in self-protection.
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Antioxidant gene expression and function in in vitro-developing Schistosoma mansoni mother sporocysts: possible role in self-protection.

机译：在体外发育的曼氏血吸虫母亲孢子囊中的抗氧化基因表达和功能：可能在自我保护中的作用。

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摘要

The ability of the larval forms of Schistosoma mansoni to invade and parasitize their molluscan host, Biomphalaria glabrata, is determined by a multitude of factors. In this study we sought to elucidate the possible mechanisms by which the invading larvae are able to counteract the potentially harmful oxidative environment presented by the host upon initial miracidial infection. This was attempted by examining the gene expression profile of parasite antioxidant enzymes of the linked glutathione-(GSH) thioredoxin (Trx) redox pathway during early intramolluscan larval development. Three such enzymes, the peroxiredoxins (Prx1, Prx2 and Prx3) were examined as to their activity and sites of expression within S. mansoni miracidia and in vitro-cultured mother sporocysts. Results of these studies demonstrated that the H(2)O(2)-reducing enzymes Prx1 and 2 are upregulated during early mother sporocyst development compared to miracidia. Immunolocalization studies further indicated that Prx1 and Prx2 proteins are expressed within the apical papillae of miracidia and tegumental syncytium of sporocysts, and are released with parasite excretory-secretory proteins (ESP) during in vitro larval transformation. Removal of Prx1 and Prx2 from larval ESP by immunoabsorption significantly reduced the ability of ESP to breakdown exogenous H(2)O(2), thereby directly linking ESP Prx proteins with H(2)O(2)-scavenging activity. Moreover, exposure of live sporocysts to exogenous H(2)O(2)stimulated an upregulation of Prx1 and 2 gene expression suggesting the involvement of H(2)O(2)-responsive elements in regulating larval Prx gene expression. These data provide evidence that Prx1 and Prx2 may function in the protection of S. mansoni sporocysts during the early stages of infection.
机译：曼氏血吸虫的幼虫形式侵袭和寄生化其软体动物寄主glaphaata glabrata的能力取决于多种因素。在这项研究中，我们试图阐明入侵的幼虫能够抵抗宿主在最初的虫感染时呈现的潜在有害氧化环境的可能机制。这是通过检查在早期软体动物幼虫发育过程中连接的谷胱甘肽-（GSH）硫氧还蛋白（Trx）氧化还原途径的寄生虫抗氧化酶的基因表达谱来进行的。检查了三种这样的酶，过氧化物酶（Prx1，Prx2和Prx3）的活性和曼氏葡萄球菌miraturia和体外培养的母孢子囊中的表达位点。这些研究的结果表明，与miraturia相比，在早期母亲孢子囊发育过程中，H（2）O（2）还原酶Prx1和2被上调。免疫定位研究进一步表明，Prx1和Prx2蛋白在水泡的顶乳头和孢子囊合胞体内表达，并在体外幼虫转化过程中与寄生虫的分泌分泌蛋白（ESP）一起释放。通过免疫吸收从幼虫ESP中去除Prx1和Prx2大大降低了ESP分解外源H（2）O（2）的能力，从而直接将ESP Prx蛋白与H（2）O（2）清除活性联系起来。此外，活的孢子囊暴露于外源H（2）O（2）刺激Prx1和2基因表达的上调，表明H（2）O（2）响应元件参与调节幼虫Prx基因表达。这些数据提供了证据，Prx1和Prx2在感染的早期阶段可能在保护曼氏葡萄球菌孢子囊中起作用。

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