Pawankar Ruby, Lee Kun Hee, Nonaka Manabu, Takizawa Ryuta
Department of Otolaryngology, Nippon Medical School, Tokyo, Japan.
Clin Allergy Immunol. 2007;20:93-101.
Mast cells and basophils contribute to induction and/or maintenance of eosinophilic inflammation by a variety of mechanisms, including IgE-dependent and IgE-independent processes. The latter include a variety of stimuli that have only recently been elucidated, including mechanisms triggered by bacteria, virus, fungi, complement, or autoantibodies. MCs, and basophils contribute to inflammation both directly through the release of inflammatory mediators, cytokines and growth factors and indirectly through the activation of structural cells. Accumulating evidence places MCs (and most probably basophils) in a position of importance in the pathogenesis of CRS, particularly in the pathogenesis and progression of NP (Fig. 1). Mechanisms other than conventional IgE-dependent activation of MCs are intriguing as potential mechanisms of eosinophilic inflammation in non-allergic CRS/NP. Although it is not possible using current pharmacologic approaches to completely isolate the effects of MCs or basophils in CRS and NP pathogenesis, it seems most likely that such approaches will eventually be available. It might be expected that one or both of these cells will be shown to play important roles, particularly considering their potential for activation by IgE and non-IgE mechanisms, their production of a broad array of inflammatory mediators, cytokines and growth factors, and their unique assortment of proteases.
肥大细胞和嗜碱性粒细胞通过多种机制促进嗜酸性粒细胞炎症的诱导和/或维持，包括IgE依赖和IgE非依赖过程。后者包括多种直到最近才被阐明的刺激因素，包括由细菌、病毒、真菌、补体或自身抗体触发的机制。肥大细胞和嗜碱性粒细胞通过释放炎症介质、细胞因子和生长因子直接促进炎症，也通过激活结构细胞间接促进炎症。越来越多的证据表明肥大细胞（很可能还有嗜碱性粒细胞）在慢性鼻-鼻窦炎（CRS）的发病机制中具有重要地位，特别是在鼻息肉（NP）的发病机制和进展中（图1）。肥大细胞的传统IgE依赖激活以外的机制作为非过敏性CRS/NP中嗜酸性粒细胞炎症的潜在机制很有意思。虽然目前使用药物方法不可能完全分离肥大细胞或嗜碱性粒细胞在CRS和NP发病机制中的作用，但似乎很可能最终会有这样的方法。可以预期，这两种细胞中的一种或两种将被证明发挥重要作用，特别是考虑到它们通过IgE和非IgE机制激活的潜力、它们产生的多种炎症介质、细胞因子和生长因子，以及它们独特的蛋白酶组合。
