枸橼酸二乙基卡马嗪对巴西尼波圆线虫感染大鼠保护性免疫的作用。

J C Katiyar, S Gupta, A B Sen
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引用次数: 0

摘要

对巴西尼波圆线虫免疫的大鼠,口服枸橼酸二乙基卡马嗪(DEC) (250 mg/kg X 6)对功能性免疫有显著抑制作用。同样,给药48/80(100微克/大鼠i.p.)使免疫大鼠易受攻击感染。用复方48/80、组胺(20 mg/只,每只)或l -组氨酸(20 mg/只,口服s.c)治疗感染22天的大鼠,并没有加速蠕虫的排出。从免疫dec治疗和未治疗的大鼠中分离的腹膜细胞(1 X 10(8))对感染性幼虫(L3)有大量补体依赖性粘附。同样,当细胞与免疫、dec处理或未处理的大鼠血清孵育时,发现正常腹膜细胞大量聚集到幼虫身上。大鼠接受从免疫dec处理的大鼠获得的肠系膜淋巴结细胞(125 × 10(6) i.v.)或血清(0.5 ml或1 ml × 3 i.p.),并用感染性幼虫攻毒,比接受未经治疗的免疫供体细胞或血清的大鼠产生的蠕虫多50%。DEC似乎引起功能性免疫的抑制,蠕虫的排出不是组胺介导的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Action of diethylcarbamazine citrate on protective immunity in rats infected with Nippostrongylus brasiliensis.

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.

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