Chiappara G, Gagliardo R, Siena A, Bonsignore M R, Bousquet J, Bonsignore G, Vignola A M
Istituto di Fisiopatologia Respiratoria, Palermo, Italy.
Curr Opin Allergy Clin Immunol. 2001 Feb;1(1):85-93. doi: 10.1097/01.all.0000010990.97765.a1.
The inflammatory and remodelling processes that underlie asthma result from a highly complex interaction between various cell types. Apart from inflammatory cells, such as eosinophils, activated T cells, mast cells and macrophages, structural tissue cells such as epithelial cells, fibroblasts and smooth muscle cells can also play an important effector role through the release of a variety of mediators, cytokines and chemokines. This results in an acute inflammatory response that is characterized by vascular leakage, mucus hypersecretion, epithelial shedding and widespread airway narrowing. At the same time, through the release of mediators, cytokines, chemokines and growth factors, epithelial and mesenchymal cells cause persistence of the inflammatory infiltrate and induce structural changes in the airway wall, such as increased thickness of the basement membrane, increased collagen deposition, changes in bronchial microcirculation, and smooth muscle hypertrophy and hyperplasia. The end result of airway inflammation and remodelling is an increased thickness of the airway wall, leading to a reduced baseline airway calibre and exaggerated airway narrowing.
哮喘所基于的炎症和重塑过程源于多种细胞类型之间高度复杂的相互作用。除了炎症细胞，如嗜酸性粒细胞、活化的T细胞、肥大细胞和巨噬细胞外，结构组织细胞，如上皮细胞、成纤维细胞和平滑肌细胞，也可通过释放多种介质、细胞因子和趋化因子发挥重要的效应作用。这会导致以血管渗漏、黏液分泌过多、上皮脱落和广泛气道狭窄为特征的急性炎症反应。同时，上皮细胞和间充质细胞通过释放介质、细胞因子、趋化因子和生长因子，导致炎症浸润持续存在，并诱导气道壁结构改变，如基底膜增厚、胶原沉积增加、支气管微循环改变以及平滑肌肥大和增生。气道炎症和重塑的最终结果是气道壁厚度增加，导致基线气道口径减小和气道狭窄加剧。
