首页> 美国卫生研究院文献>Clinical and Experimental Immunology >Dipetalonema viteae infective larvae reach reproductive maturity in rats immunodepressed by prior exposure to Schistosoma mansoni or its products and in congenitally athymic rats
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Dipetalonema viteae infective larvae reach reproductive maturity in rats immunodepressed by prior exposure to Schistosoma mansoni or its products and in congenitally athymic rats

机译:在事先暴露于曼氏血吸虫或其产物后被免疫抑制的大鼠和先天性无胸腺大鼠中铁皮双足蜂感染的幼虫达到了生殖成熟。

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摘要

Infective larvae of Dipetalonema viteae did not reach maturity in inbred Fischer rats. However, female adults of D. viteae 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 Schistosoma mansoni infection or by treatment with S. mansoni-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 S. mansoni on the survival and growth of D. viteae in Fischer rats depends greatly on the relative timing of infection because infective larvae of D. viteae reached maturity only when rats were inoculated with infective larvae after 15 days of S. mansoni infection but not after 21 or 28 days of S. mansoni infection. D. viteae 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.
机译:在Fischer近交大鼠中,Dipetalonema viteae的感染性幼虫未达到成熟。但是,建立了经手术移植到Fischer大鼠体内的D. viteae成年雌性,感染后的蠕虫产生的微丝虫病持续了约120天。顺序解剖显示,感染后一些雌性蠕虫在大鼠中存活约35天。将感染性幼虫接种到大鼠中后,不同数量的幼虫转化为4期幼虫,但它们没有发育成成虫,并被杀死。但是,当大鼠被预先存在的曼氏血吸虫感染或通过曼氏葡萄球菌衍生的物质治疗而受到非特异性免疫抑制时,许多第4阶段幼虫恢复了发育并达到了性成熟。这些蠕虫产生微丝虫病,在外周血中观察到约40天。先前感染曼氏沙门氏菌对费歇尔大鼠D. viteae存活和生长的影响在很大程度上取决于相对的感染时机,因为仅在15天的感染后将D. viteae的感染性幼虫接种到大鼠中,D。viteae的感染性幼虫才达到成熟。曼氏沙门氏菌感染,但在曼氏沙门氏菌感染21或28天后没有。在先天性无胸腺大鼠中,D。viteae也将发育成熟。在先天性无胸腺大鼠(Nu / Nu)中,每只给予75只感染性幼虫,死后的微丝虫病和成虫的恢复均高于导致Nu / Nu鼠受到200只幼虫感染的鼠。这些实验表明,在大鼠中,对这种丝虫线虫的先天免疫力反映了非常迅速诱导的获得性免疫力,该免疫力在寄生虫成熟之前将其杀死。

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