An essential role for interleukin-5 and eosinophils in helminth-induced airway hyperresponsiveness.
An essential role for interleukin-5 and eosinophils in helminth-induced airway hyperresponsiveness.
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白细胞介素 5 和嗜酸性粒细胞在蠕虫引起的气道高反应性中发挥重要作用。
DOI：
10.1128/iai.66.9.4425-4430.1998
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发表时间：
1998
影响因子：
3.1
通讯作者：
Pearlman,E
中科院分区：
文献类型：
--
作者：
Hall,LR;Mehlotra,RK;Higgins,AW;Haxhiu,MA;Pearlman,E
感染马来丝虫可引起严重的哮喘反应，称为热带肺嗜酸性粒细胞增多症。这种疾病被认为是由于宿主对血液寄生虫的炎症反应而引起的，血液寄生虫被困在肺微血管中，其特征在于嗜酸性粒细胞严重浸润到肺中。嗜酸性粒细胞的募集也与对胆碱能激动剂的气道高反应性（AHR）和严重哮喘症状的发生相关。我们的研究探讨了白细胞介素-5（IL-5）在蠕虫诱导的肺嗜酸性粒细胞增多症和AHR中的作用。用灭活B. Malayimicrofilariae感染和用活微丝蚴静脉内攻击显示出许多人类疾病的特征，包括外周和肺嗜酸性粒细胞增多。致敏小鼠支气管肺泡灌洗回收的细胞在激发后第1天为3.8%，第10天为84%。细胞外主要碱性蛋白早在第1天就存在于气道上皮细胞表面，8天后继续明显，表明肺中嗜酸性粒细胞的持续活化和脱粒。这些组织学变化与AHR向卡巴胆碱的发展相关。与免疫活性小鼠相比，B. malayin IL-5−/−小鼠没有诱导外周或肺嗜酸性粒细胞增多，这些小鼠对胆碱能激动剂的反应也没有表现出AHR。总之，这些数据表明，IL-5和嗜酸性粒细胞所需的诱导AHR的丝虫蠕虫。
Infection with the parasitic helminthBrugia malayican result in development of a severe asthmatic response termed tropical pulmonary eosinophilia. This disease, thought to result from a host inflammatory response to blood parasites which become trapped in the lung microvasculature, is characterized by a profound eosinophilic infiltration into the lungs. Recruitment of eosinophils also correlates with the development of airway hyperresponsiveness (AHR) to cholinergic agonists and severe asthmatic symptoms. Our studies examined the role of interleukin-5 (IL-5) in helminth-induced pulmonary eosinophilia and AHR. C57BL/6 mice immunized with killedB. malayimicrofilariae and challenged intravenously with live microfilariae exhibit many of the characteristics of human disease, including peripheral and pulmonary eosinophilia. Cells recovered by bronchoalveolar lavage of sensitized mice consisted of 3.8% eosinophils on day 1 postchallenge and 84% on day 10. Extracellular major basic protein was present on the surface of airway epithelial cells as early as day 1 and continued to be evident after 8 days, indicating sustained activation and degranulation of eosinophils in the lung. These histologic changes correlated with the development of AHR to carbachol. In contrast to immunocompetent mice, immunization and challenge withB. malayiin IL-5−/−mice did not induce peripheral or pulmonary eosinophilia, and these mice failed to show AHR in response to cholinergic agonists. Taken together, these data indicate that IL-5 and eosinophils are required for the induction of AHR by filarial helminths.