Antigen-induced airway hyperresponsiveness, pulmonary eosinophilia, and chemokine expression in B cell-deficient mice
Antigen-induced airway hyperresponsiveness, pulmonary eosinophilia, and chemokine expression in B cell-deficient mice
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DOI：
10.1165/ajrcmb.20.3.3291
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发表时间：
1999-03-01
影响因子：
6.4
通讯作者：
De Sanctis, GT
中科院分区：
文献类型：
--
作者：
MacLean, JA;Sauty, A;De Sanctis, GT
过敏原诱导的肺部炎症的小鼠模型与人类哮喘具有许多共同特征，包括抗原诱导的肺嗜酸性粒细胞增多症、气道高反应性、抗原特异性细胞和抗体应答、Th 2细胞因子（白细胞介素[IL]-4和IL-5）的产生以及具有嗜酸性粒细胞活性的趋化因子的表达。我们研究了B细胞和抗原特异性抗体反应在这样一个模型中的作用，通过研究B细胞缺陷小鼠的组织病理学和生理反应，与野生型对照组相比，系统免疫和用卵清蛋白（OVA）的气道挑战。OVA攻击的野生型和B细胞缺陷小鼠均出现（1）气道高反应性，（2）T细胞和嗜酸性粒细胞活化的肺部炎症，（3）IL-4和IL-5分泌到气道腔中，以及（4）嗜酸性粒细胞活性趋化因子eotaxin和单核细胞趋化蛋白-3的表达增加。与野生型小鼠相比，B细胞缺陷小鼠的病理或生理反应均无显著差异。这些数据表明，B细胞和抗原特异性抗体的气道高反应性，嗜酸性粒细胞性肺部炎症，和趋化因子的表达在致敏小鼠的抗原气雾剂攻击后的发展是不需要的。
Murine models of allergen-induced pulmonary inflammation share many features with human asthma, including the development of antigen-induced pulmonary eosinophilia, airway hyperresponsiveness, antigen-specific cellular and antibody responses, the elaboration of Th2 cytokines (interleukin [IL]-4 and IL-5), and the expression of chemokines with activity for eosinophils. We examined the role of B cells and antigen-specific antibody responses in such a model by studying the histopathologic and physiologic responses of B cell-deficient mice compared with wild-type controls, following systemic immunization and airway challenge with ovalbumin (OVA). Both OVA-challenged wild-type and B cell-deficient mice developed (1) airway hyperresponsiveness, (2) pulmonary inflammation with activated T cells and eosinophils, (3) IL-4 and IL-5 secretion into the airway lumen, and (4) increased expression of the eosinophil active chemokines eotaxin and monocyte chemotactic protein-3. There were no significant differences in either the pathologic or physiologic responses in the B cell-deficient mice compared with wild-type mice. These data indicate that B cells and antigen-specific antibodies are not required for the development of airway hyperresponsiveness, eosinophilic pulmonary inflammation, and chemokine expression in sensitized mice following aerosol challenge with antigen.