Late pulmonary allergic responses in actively but not passively IgE-sensitized rats.
Late pulmonary allergic responses in actively but not passively IgE-sensitized rats.
复制标题
主动而非被动 IgE 致敏大鼠的晚期肺部过敏反应。
DOI：
10.1152/jappl.1990.69.3.1012
复制
发表时间：
1990
期刊：
影响因子：
--
通讯作者：
LemanskeJr,RF
中科院分区：
文献类型：
--
作者：
Sorkness,R;Johns,K;Castleman,WL;LemanskeJr,RF
先前的研究表明，尽管被动致敏[单克隆鼠免疫球蛋白E（IgE）]的大鼠对肺抗原激发的反应会立即增加抵抗力，但与主动致敏优先产生IgE抗体的大鼠的晚期变化不同，它们没有表现出晚期抵抗力增加。我们假设被动致敏大鼠也不会发生抗原诱导的肺部炎症。在盲法方案中，我们比较了立即反应和肺阻力和炎症后8，19和24小时的挑战与安慰剂抗原，与二硝基苯酚-牛血清白蛋白（DNP-BSA），以引起被动致敏反应，或与卵清蛋白（OA），以引起主动致敏反应。尽管对OA和DNP-BSA有类似的即时反应，但只有OA激发的大鼠有明显的炎症变化和晚期抵抗力升高的显著发生率。炎症评分和肺阻力仅在OA组中显著相关。我们还观察到，与氯胺酮麻醉的大鼠相比，芬太尼/氟哌利多麻醉显著减弱了对抗原激发的即时反应，但不减弱晚期反应。我们的结论是IgE介导的肺抗原激发的即时反应是不够的，可能是不必要的，启动抗原诱导的晚期炎症变化。
Previous studies suggested that although rats that were passively sensitized [monoclonal murine immunoglobulin E (IgE)] would respond to pulmonary antigen challenge with an immediate increase in resistance, they exhibited no late increases in resistance, unlike late changes in rats actively sensitized to preferentially produce IgE antibody. We hypothesized that passively sensitized rats also would not develop antigen-induced pulmonary inflammation. In a blinded protocol we compared immediate responses and pulmonary resistance and inflammation at 8, 19 and 24 h after challenge with placebo antigen, with dinitrophenol-bovine serum albumin (DNP-BSA) to elicit a passively sensitized response, or with ovalbumin (OA) to elicit an actively sensitized response. Despite similar immediate responses to OA and DNP-BSA, only the rats challenged with OA had marked inflammatory changes and a significant incidence of late elevations in resistance. Inflammation scores and lung resistance were significantly correlated only in the OA group. We also observed that anesthesia with fentanyl/droperidol significantly attenuated the immediate but not the late responses to antigen challenge, compared with rats anesthetized with ketamine. We conclude that IgE-mediated immediate responses to pulmonary antigen challenge are insufficient, and may be unnecessary, to initiate antigen-induced late inflammatory changes.