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Immediate hypersensitivity reactions in epithelia from rats infected with Nippostrongylus brasiliensis.

机译:感染巴西拟夜蛾的大鼠上皮立即发生超敏反应。

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摘要

Colonic epithelia from rats infected with the nematode Nippostrongylus brasiliensis have been studied under short circuit conditions and in response to challenge with worm antigen. Challenge from the serosal but not the mucosal side with antigen caused a transient increase in inwardly directed short circuit current. No effects were observed in comparable tissues from noninfected animals. Simultaneous measurements of short circuit current and of the fluxes of sodium or chloride ions showed there was an increase in electrogenic chloride secretion and an inhibition of electroneutral sodium chloride absorption, associated with antigen challenge. This result, together with the inhibitory effects of piretanide on the response to antigen challenge, indicate that chloride ions are a major carrier of the short circuit current response. However, the equivalence of the biophysical response to ion fluxes was not established, there being an excess of chloride secretion. The mast cell stabilizing agent, FPL 52694, significantly inhibited the current responses to antigen, while cromoglycate and doxantrazole were ineffective. Mepyramine, an H1-receptor antagonist, and indomethacin, an inhibitor of fatty acid cyclo-oxygenase, were without effect on the responses to antigen challenge. Anti-rat IgE produced qualitatively similar responses to antigen in both normal and sensitized colonic epithelia. However, the responses were significantly greater in tissues derived from infected animals. Maximally effective antigen concentrations prevented subsequent responses to anti-rat IgE in sensitized tissues, while anti-rat IgE only attenuated the responses to antigen. The ways in which antigen challenge modifies epithelial function is discussed, particularly in relation to its possible role in promoting rejection of the nematodes during secondary infection.
机译:已经在短路条件下以及响应蠕虫抗原的攻击下研究了感染了巴西线虫日本线虫的大鼠的结肠上皮。来自抗原的浆膜侧而非粘膜侧的刺激引起向内定向的短路电流的瞬时增加。在未感染动物的可比较组织中未观察到影响。同时测量短路电流以及钠离子或氯离子的通量表明,与抗原攻击有关的电氯化物分泌增加,并且抑制了电中性氯化钠吸收。该结果以及吡咯他尼对抗原激发反应的抑制作用表明,氯离子是短路电流反应的主要载体。但是,尚未建立对离子通量的生物物理反应的等价物,因为氯化物的分泌过多。肥大细胞稳定剂FPL 52694显着抑制了对抗原的电流反应,而色甘酸和多沙坦唑无效。 Mepyramine(一种H1受体拮抗剂)和吲哚美辛(一种脂肪酸环加氧酶的抑制剂)对抗原攻击的反应没有影响。在正常和致敏的结肠上皮中,抗大鼠IgE对抗原的定性反应相似。但是,在源自感染动物的组织中,反应明显更大。最大有效抗原浓度阻止了敏化组织对抗大鼠IgE的后续反应,而抗大鼠IgE仅减弱了对抗原的反应。讨论了抗原攻击修饰上皮功能的方式,特别是关于其在继发感染过程中促进线虫排斥的可能作用。

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