The effect of segmental bronchoprovocation with allergen on airway lymphocyte function
The effect of segmental bronchoprovocation with allergen on airway lymphocyte function
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DOI：
10.1164/ajrccm.156.5.9703054
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发表时间：
1997-11-01
影响因子：
24.7
通讯作者：
Jarjour, NN
中科院分区：
文献类型：
--
作者：
Kelly, EAB;Rodriguez, RR;Jarjour, NN
我们假设过敏原诱导的气道嗜酸性粒细胞增多与气道中T细胞的激活或募集以及白细胞介素-5 （IL-5）的产生有关。为了评估这一假设，我们对12名特应性受试者进行了段性抗原支气管激发的支气管镜检查。分别在生理盐水或抗原刺激后5分钟和48小时进行支气管肺泡灌洗（BAL）。分离气道细胞，然后体外用t细胞有丝分裂原、植物血凝素（PHA）刺激，并测定细胞因子的释放。从盐胁迫段提取的细胞主要分泌干扰素- γ (ifn - γ)和IL-2。相比之下，在过敏原攻击48小时后获得的细胞分泌高水平的IL-5和少量但增加的IL-4、IL-10和粒细胞-巨噬细胞集落刺激因子（GM-CSF）。虽然CD4(+) T细胞是IL-5的主要来源，但在支气管刺激反应中，CD4（+）细胞的相对比例没有显著变化。此外，气道细胞体外分泌IL-5与支气管肺泡灌洗液（BALF）中IL-5和嗜酸性粒细胞的含量密切相关。这些观察结果表明，暴露于过敏原后，气道T细胞在功能上但在表型上与常驻气道T细胞不同，气道内的T细胞通过分泌IL-5参与嗜酸性气道炎症。
We hypothesized that allergen-induced airway eosinophilia is linked to activation or recruitment of T cells in the airway and generation of interleukin-5 (IL-5). To evaluate this hypothesis, we performed bronchoscopy with segmental antigen bronchoprovocation in 12 atopic subjects. Bronchoalveolar lavage (BAL) was done 5 min and 48 h after challenge with saline or antigen. Airway cells were isolated and then stimulated ex vivo with a T-cell mitogen, phytohemagglutinin (PHA), and cytokine release was determined. Cells retrieved from the saline-challenged segment secreted principally interferon-gamma (IFN-gamma) and IL-2. In contrast, cells obtained 48 h after allergen challenge secreted high levels of IL-5 and small but increased amounts of IL-4, IL-10, and granulocyte-macrophage colony-stimulating factor (GM-CSF). Although CD4(+) T cells were a major source of IL-5, there were no significant changes in the relative proportion of CD4(+) cells in response to bronchoprovocation. Additionally, ex vivo secretion of IL-5 by airway cells correlated closely with amounts of IL-5 and eosinophils present in the bronchoalveolar lavage fluid (BALF). These observations suggest that following exposure to allergen, airway T cells are functionally but not phenotypically different from resident airway T cells, and that T cells within the airway contribute to eosinophilic airway inflammation through the secretion of IL-5.