When asthma is diagnosed, eosinophilic inflammation and airway remodeling are established in the bronchial airways and can no longer be separated as cause and effect because both processes contribute to persistence and progression of disease, despite anti-inflammatory therapy. Th2 cells are continually active in the airways, even when disease is quiescent. IL-13 is the key effector cytokine in asthma and stimulates airway fibrosis through the action of matrix metalloproteinases on TGF-beta and promotes epithelial damage, mucus production, and eosinophilia. The production of IL-13 and other Th2 cytokines by non-T cells augments the inflammatory response. Inflammation is amplified by local responses of the epithelium, smooth muscle, and fibroblasts through the production of chemokines, cytokines, and proteases. Injured cells produce adenosine that enhances IL-13 production. We review human and animal data detailing the cellular and molecular interactions in established allergic asthma that promote persistent disease, amplify inflammation, and, in turn, cause disease progression.

中文翻译：

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哮喘：疾病持续和进展的机制。

当诊断出哮喘时，在支气管气道中建立了嗜酸性炎症和气道重塑，由于抗炎治疗，尽管这两个过程都有助于疾病的持久性和进展，但不能再将其作为因果关系分开。Th2细胞在呼吸道中持续活跃，即使疾病处于静止状态也是如此。IL-13是哮喘中的关键效应细胞因子，通过基质金属蛋白酶对TGF-β的作用刺激气道纤维化，并促进上皮损伤，粘液产生和嗜酸性粒细胞增多。非T细胞产生IL-13和其他Th2细胞因子会增强炎症反应。通过产生趋化因子，细胞因子和蛋白酶，上皮，平滑肌和成纤维细胞的局部反应会加剧炎症。受伤的细胞产生腺苷，可增强IL-13的产生。我们审查了人类和动物的数据，这些数据详细说明了已建立的变应性哮喘中细胞和分子的相互作用，从而促进持续性疾病，加剧炎症并进而导致疾病进展。