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枸橼酸乙胺嗪对感染巴西日圆线虫大鼠保护性免疫的作用

Action of diethylcarbamazine citrate on protective immunity in rats infected with Nippostrongylus brasiliensis.

作者信息

Katiyar J C, Gupta S, Sen A B

出版信息

Z Parasitenkd. 1985;71(3):401-8. doi: 10.1007/BF00928342.

Abstract

Rats made immune to Nippostrongylus brasiliensis and treated with diethylcarbamazine citrate (DEC) orally (250 mg/kg X 6) exhibited significant suppression of functional immunity. Similarly, administration of compound 48/80 (100 micrograms/rat i.p.) made the immune rats susceptible to challenge infection. Treatment of rats, with 22-day infection with compound 48/80, histamine (20 mg/rat, per os), or L-histidine (20 mg/rat, orally s.c.) did not accelerate worm expulsion. A massive complement-dependent adherence of peritoneal cells (1 X 10(8], isolated from immune DEC-treated and untreated rats, to infective larvae (L3) was observed. Likewise, heavy congregation of normal peritoneal cells to larvae was noticed when the cells were incubated with sera obtained from immune, DEC-treated or untreated rats. The rats receiving mesenteric lymph node cells (125 X 10(6) i.v.) or sera (0.5 ml or 1 ml X 3 i.p.), obtained from immune DEC-treated rats and challenged with infective larvae developed 50% more worms than those which received cells or serum from untreated immune donors. DEC appears to cause suppression of functional immunity and worm expulsion is not histamine mediated.

摘要

对巴西日圆线虫产生免疫的大鼠经口给予枸橼酸乙胺嗪(DEC)(250mg/kg×6)后,其功能性免疫受到显著抑制。同样,给予化合物48/80(100μg/大鼠,腹腔注射)会使免疫大鼠易于受到攻击感染。用化合物48/80、组胺(20mg/大鼠,经口)或L-组氨酸(20mg/大鼠,口服或皮下注射)对感染22天的大鼠进行处理,并未加速蠕虫排出。观察到从经DEC处理和未处理的免疫大鼠分离的腹膜细胞(1×10⁸)对感染性幼虫(L3)有大量补体依赖性黏附。同样,当正常腹膜细胞与从免疫、经DEC处理或未处理的大鼠获得的血清一起孵育时,会注意到细胞大量聚集在幼虫周围。接受从经DEC处理的免疫大鼠获得的肠系膜淋巴结细胞(125×10⁶,静脉注射)或血清(0.5ml或1ml×3,腹腔注射)并用感染性幼虫攻击的大鼠,其体内蠕虫数量比接受未处理的免疫供体的细胞或血清的大鼠多50%。DEC似乎会导致功能性免疫受到抑制,并且蠕虫排出不是由组胺介导的。

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