アレルギー性気道炎症におけるAT II la受容体の機能解析

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Chronic airway inflammation and airway hyperresponsiveness (AHR) are fundamental features leading to airway narrowing in bronchial asthma. Airway inflammation in asthmatics is characterized with the accumulation and activation of inflammatory cells such as eosinophils and mast cells, which is orchestrated by a network of Th2 cytokines, such as IL-4 and IL-5, released mainly from CD^+_4 T lymphocytes. The peptide hormone angiotensin II (AT II) plays an important role in the regulation of arterial blood pressure. Plasma levels of renin and AT II were reported to be elevated during acute exacerbation of asthma, and studies using type 1 AT II receptor (AT1) antagonist (ARE) suggested the involvement of the receptor in the pathogenesis of asthma. However, the pathogenic roles of AT II and AT1 in asthmatic airway inflammation remains elusive. Therefore, we investigated the effect of ATla gene deletion (ATlaKO) on allergen-induced airway inflammation using a murine model of allergic asthma. In sensitized wild type mice (WT), the numbers of inflammatory cells in bronchoalveolar lavage fluids (BALF) were increased with a peak on 5 days after antigen challenge. In ATlaKO mice, in contrast, those were increased with two peaks on 3 and 7 days, which were significantly higher than in WT. The contents of IL-4 and IL-5 in BALF of ATlaKO mice 1 day after the challenge were significantly higher than those of WT mice. These date suggest that ATla play a pivotal role in allergic airway inflammation via, at least in part, the downregulation of Th2 cytokine expression.

アレルギー性気道炎症におけるAT II la受容体の機能解析

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