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双瓣棘唇线虫感染性幼虫在先前接触过曼氏血吸虫或其产物而免疫抑制的大鼠以及先天性无胸腺大鼠体内达到生殖成熟。

Dipetalonema viteae infective larvae reach reproductive maturity in rats immunodepressed by prior exposure to Schistosoma mansoni or its products and in congenitally athymic rats.

作者信息

Haque A, Camus D, Ogilvie B M, Capron M, Bazin H, Capron A

出版信息

Clin Exp Immunol. 1981 Jan;43(1):1-9.

Abstract

Infective larvae of did not reach maturity in inbred Fischer rats. However, female adults of when transplanted surgically into Fischer rats established and the resulting microfilaraemia from the transplanted worms persisted for about 120 days after infection. Sequential dissections showed that some of the female worms transplanted remained viable in rats for about 35 days after infection. After inoculation of infective larvae into rats a varying number transformed into stage-4 larvae but they did not develop into adult worms and were killed. However, when the rats were immunodepressed non-specifically by a pre-existing infection or by treatment with -derived substance(s), a number of stage-4 larvae renewed their development and reached sexual maturity. These worms produced microfilariae which were observed in the peripheral blood for about 40 days. The effect of previous infection with on the survival and growth of in Fischer rats depends greatly on the relative timing of infection because infective larvae of reached maturity only when rats were inoculated with infective larvae after 15 days of infection but not after 21 or 28 days of infection. will also develop to maturity in congenitally athymic rats. In congenitally athymic rats (Nu/Nu) each given 75 infective larvae, both the microfilaraemia and adult worm recovery at post-mortem were higher than those which resulted in Nu/Nu rats given an infection of 200 larvae. These experiments show that in rats innate immunity to this filarial nematode reflects a very rapidly induced acquired immunity which kills the parasite before it reaches maturity.

摘要

在近交系Fischer大鼠中,[寄生虫名称]的感染性幼虫未发育成熟。然而,将[寄生虫名称]的雌性成虫手术移植到Fischer大鼠体内后,它们得以存活,并且感染后由移植蠕虫产生的微丝蚴血症持续了约120天。连续解剖显示,一些移植的雌性蠕虫在感染后约35天内在大鼠体内仍存活。将感染性幼虫接种到大鼠体内后,不同数量的幼虫转化为4期幼虫,但它们未发育为成虫并被杀死。然而,当大鼠因先前存在的[感染源名称]感染或用[物质名称]衍生物质进行治疗而非特异性免疫抑制时,一些4期幼虫恢复发育并达到性成熟。这些蠕虫产生了微丝蚴,在周围血液中观察到约40天。先前感染[感染源名称]对Fischer大鼠体内[寄生虫名称]的存活和生长的影响在很大程度上取决于感染的相对时间,因为只有当大鼠在[感染源名称]感染15天后接种感染性幼虫时,[寄生虫名称]的感染性幼虫才会发育成熟,而在[感染源名称]感染21天或28天后接种则不会。[寄生虫名称]在先天性无胸腺大鼠中也会发育成熟。在每只接种75条感染性幼虫的先天性无胸腺大鼠(Nu/Nu)中,死后的微丝蚴血症和成虫回收率均高于接种200条幼虫的Nu/Nu大鼠。这些实验表明,在大鼠中,对这种丝虫线虫的先天免疫反映了一种诱导非常迅速的获得性免疫,该免疫在寄生虫成熟之前将其杀死。

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