Zhang S, Castro G A
Department of Physiology and Cell Biology, University of Texas Medical School, Houston.
Int Arch Allergy Appl Immunol. 1990;93(2-3):272-9. doi: 10.1159/000235313.
The role of type I hypersensitivity in the rapid rejection of Trichinella spiralis from actively and passively immunized rats was examined. Net intestinal fluid secretion, which occurs during the rejection of the parasites, was used to verify the expression of local anaphylaxis and was examined for its possible role in the rejection process. Worm establishment in the small intestine 30 min after intraduodenal inoculation was significantly reduced in rats that were passively immunized with immune serum containing anti-Trichinella IgE as compared with recipients of normal serum. Worm-induced fluid secretion in immune rats was completely inhibited by the combined action of indomethacin and diphenhydramine. However, worm rejection was not affected. L-651,392, a 5-lipoxygenase inhibitor, also failed to prevent rejection. Ketanserin (a serotonin S2 receptor antagonist) and MDL-72222 (a serotonin S3 receptor antagonist) together blunted the rapid rejection response and reduced fluid secretion. Furthermore, intra-arterial perfusion of serotonin into nonimmune rats caused fluid secretion and reduced worm establishment. In nonimmune rats prostaglandin E2, cholera toxin, and hypertonic Krebs-mannitol solution were used to evoke the same level of intestinal fluid secretion as that induced by reinfection in immune rats or by serotonin in nonimmune hosts. When larvae were inoculated into the secreting gut, their infectivity was unaffected. The results suggest that anaphylaxis is involved in the rapid rejection of T. spiralis in immune rats and that serotonin is a possible chemical mediator of worm rejection. Although the mode of action of serotonin in the rejection process remains unknown, its possible involvement through fluid secretion can be ruled out.
研究了I型超敏反应在主动和被动免疫大鼠快速排斥旋毛虫中的作用。在寄生虫排斥过程中出现的净肠液分泌，被用于验证局部过敏反应的表现，并研究其在排斥过程中的可能作用。与接受正常血清的大鼠相比，用含有抗旋毛虫IgE的免疫血清被动免疫的大鼠，十二指肠内接种30分钟后小肠内虫体的定植显著减少。吲哚美辛和苯海拉明的联合作用完全抑制了免疫大鼠中虫体诱导的液体分泌。然而，虫体排斥未受影响。5-脂氧合酶抑制剂L-651,392也未能阻止排斥反应。酮色林（一种5-羟色胺S2受体拮抗剂）和MDL-72222（一种5-羟色胺S3受体拮抗剂）共同减弱了快速排斥反应并减少了液体分泌。此外，向非免疫大鼠动脉内灌注5-羟色胺会引起液体分泌并减少虫体定植。在非免疫大鼠中，前列腺素E2、霍乱毒素和高渗克雷布斯-甘露醇溶液被用于引发与免疫大鼠再次感染或非免疫宿主中5-羟色胺诱导的相同水平的肠液分泌。当幼虫接种到分泌肠中时，它们的感染力不受影响。结果表明，过敏反应参与了免疫大鼠中旋毛虫的快速排斥，并且5-羟色胺是虫体排斥的一种可能化学介质。尽管5-羟色胺在排斥过程中的作用方式尚不清楚，但其通过液体分泌的可能参与可以排除。
