Borish L
Department of Medicine, New England Medical Center, Boston, MA 02111.
Immunol Invest. 1987 Oct;16(6):501-32. doi: 10.3109/08820138709087099.
In summary, these observations suggest a model for asthma which is summarized in Table III. Initially, mast cells and possibly other bronchial cells, e.g., alveolar macrophages, are activated either in an IgE-dependent or, in intrinsic asthma, in an IgE-independent fashion. These cells release two sets of mediators which may be either preformed or newly synthesized. One set of mediators is responsible for the immediate bronchospastic response. This bronchospasm is transient, readily reversible, and not associated with either airway inflammation or bronchial hyperreactivity. The second set of mediators, however, promote chemotaxis and activation of neutrophils and eosinophils. The subsequent bronchial inflammation causes damage and desquamation of the respiratory epithelium. The increased exposure of irritant receptors results in hyperreactive airways. In addition, these inflammatory cells induce mast cell degranulation and recurrent bronchospasm. Thus, after the initial exposure to allergen, a vicious cycle of inflammation, hyperreactivity and recurrent mast cell degranulation develops, ultimately leading to the pathological picture of chronic asthma.
总之，这些观察结果提示了一种哮喘模型，总结于表III。最初，肥大细胞以及可能的其他支气管细胞，如肺泡巨噬细胞，以IgE依赖的方式或在内源性哮喘中以IgE非依赖的方式被激活。这些细胞释放两组介质，它们可以是预先形成的或新合成的。一组介质负责即刻的支气管痉挛反应。这种支气管痉挛是短暂的、易于逆转的，且与气道炎症或支气管高反应性均无关。然而，第二组介质促进中性粒细胞和嗜酸性粒细胞的趋化和激活。随后的支气管炎症导致呼吸道上皮损伤和脱落。刺激感受器暴露增加导致气道高反应性。此外，这些炎症细胞诱导肥大细胞脱颗粒和反复的支气管痉挛。因此，在最初接触过敏原后，炎症、高反应性和反复肥大细胞脱颗粒的恶性循环形成，最终导致慢性哮喘的病理表现。
