Takeda K, Hamelmann E, Joetham A, Shultz L D, Larsen G L, Irvin C G, Gelfand E W
Division of Basic Sciences and Pulmonary Medicine, Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado, USA.
J Exp Med. 1997 Aug 4;186(3):449-54. doi: 10.1084/jem.186.3.449.
Mast cells are the main effector cells of immediate hypersensitivity and anaphylaxis. Their role in the development of allergen-induced airway hyperresponsiveness (AHR) is controversial and based on indirect evidence. To address these issues, mast cell-deficient mice (W/W v) and their congenic littermates were sensitized to ovalbumin (OVA) by intraperitoneal injection and subsequently challenged with OVA via the airways. Comparison of OVA-specific immunoglobulin E (IgE) levels in the serum and numbers of eosinophils in bronchoalveolar lavage fluid or lung digests showed no differences between the two groups of mice. Further, measurements of airway resistance and dynamic compliance at baseline and after inhalation of methacholine were similar. These data indicate that mast cells or IgE-mast cell activation is not required for the development of eosinophilic inflammation and AHR in mice sensitized to allergen via the intraperitoneal route and challenged via the airways.
肥大细胞是速发型超敏反应和过敏反应的主要效应细胞。它们在变应原诱导的气道高反应性（AHR）发展中的作用存在争议且基于间接证据。为解决这些问题，将肥大细胞缺陷小鼠（W/W v）及其同基因同窝小鼠通过腹腔注射对卵清蛋白（OVA）进行致敏，随后经气道用OVA进行激发。血清中OVA特异性免疫球蛋白E（IgE）水平以及支气管肺泡灌洗液或肺消化液中嗜酸性粒细胞数量的比较显示两组小鼠之间无差异。此外，基线时以及吸入乙酰甲胆碱后的气道阻力和动态顺应性测量结果相似。这些数据表明，对于经腹腔途径致敏并经气道激发的变应原致敏小鼠，嗜酸性粒细胞炎症和AHR的发展不需要肥大细胞或IgE-肥大细胞激活。
