Interleukin 5 deficiency abolishes eosinophilia, airways hyperreactivity, and lung damage in a mouse asthma model.
Interleukin 5 deficiency abolishes eosinophilia, airways hyperreactivity, and lung damage in a mouse asthma model.
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白介素5缺乏消除小鼠哮喘模型中的嗜酸性粒细胞，气道高反应性和肺损伤。
DOI：
10.1084/jem.183.1.195
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发表时间：
1996-01-01
影响因子：
15.3
通讯作者：
Young, IG
中科院分区：
文献类型：
--
作者：
Foster, PS;Hogan, SP;Ramsay, AJ;Matthaei, KI;Young, IG
气道炎症被认为在哮喘的发病机制中起核心作用。然而，个别炎症细胞和介质在气道高反应性的发展中发挥的确切作用以及过敏性肺部炎症期间肺的形态学变化尚不清楚。在这项调查中，我们已经使用了过敏性肺部炎症和白细胞介素（IL）5缺乏小鼠的小鼠模型，以建立这种细胞因子和嗜酸性粒细胞在开始的吸入性过敏原诱导的肺损伤和气道高反应性的发展中的重要作用。致敏和卵清蛋白的小鼠气溶胶激发导致气道嗜酸性粒细胞增多和广泛的肺损伤，类似于哮喘中所见。吸入过敏原的小鼠也表现出气道对β-乙酰甲胆碱的高反应性。在IL-5缺陷小鼠中，通常由空气过敏原激发引起的嗜酸性粒细胞增多、肺损伤和气道高反应性被消除。用重组牛痘病毒重建IL-5的生产，表达这种因子，完全恢复了空气过敏原诱导的嗜酸性粒细胞增多症和气道功能障碍。这些结果表明，IL-5和嗜酸性粒细胞是过敏性肺疾病发病机制中的中心介质。
Airways inflammation is thought to play a central role in the pathogenesis of asthma. However, the precise role that individual inflammatory cells and mediators play in the development of airways hyperreactivity and the morphological changes of the lung during allergic pulmonary inflammation is unknown. In this investigation we have used a mouse model of allergic pulmonary inflammation and interleukin (IL) 5-deficient mice to establish the essential role of this cytokine and eosinophils in the initiation of aeroallergen-induced lung damage and the development of airways hyperreactivity. Sensitization and aerosol challenge of mice with ovalbumin results in airways eosinophilia and extensive lung damage analogous to that seen in asthma. Aeroallergen-challenged mice also display airways hyperreactivity to beta-methacholine. In IL-5-deficient mice, the eosinophilia, lung damage, and airways hyperreactivity normally resulting from aeroallergen challenge were abolished. Reconstitution of IL-5 production with recombinant vaccinia viruses engineered to express this factor completely restored aeroallergen-induced eosinophilia and airways dysfunction. These results indicate that IL-5 and eosinophils are central mediators in the pathogenesis of allergic lung disease.
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影响因子：
5.5
作者：
KURUP, VP;CHOI, HY;COFFMAN, RL
通讯作者：
COFFMAN, RL
影响因子：
56.9
作者：
RAMSAY, AJ;HUSBAND, AJ;KOPF, M
通讯作者：
KOPF, M
DOI：
10.1164/ajrccm/139.3.806
发表时间：
1989-03-01
期刊：
AMERICAN REVIEW OF RESPIRATORY DISEASE
影响因子：
--
作者：
BEASLEY, R;ROCHE, WR;HOLGATE, ST
通讯作者：
HOLGATE, ST
影响因子：
56.9
作者：
COFFMAN, RL;SEYMOUR, BWP;RENNICK, D
通讯作者：
RENNICK, D
影响因子：
15.9
作者：
HAMID, Q;AZZAWI, M;KAY, AB
通讯作者：
KAY, AB