Inflammation in Asthma Pathogenesis: Role of T Cells, Macrophages, Epithelial Cells and Type 2 Inflammation.

Abstract

Asthma is a chronic disease with abnormal inflammatory and immunological responses. The disease initiates by antigens in subjects with genetic susceptibility. However, environmental factors play a role in the initiation and exacerbation of asthma attack. Asthma is a T-helper 2 (Th2)-cell-mediated disease. Recent studies indicate that asthma is not a single disease entity, but it occurs with multiple phenotypes and endotypes. The pathophysiological changes in asthma include a series of continuous vicious circles of cellular activation contributing to the induction of chemokines and cytokines that potentiate inflammation. The heterogeneity of asthma influences the treatment response. The asthma pathogenesis is driven by varied sets of cells, such as eosinophils, basophils, neutrophils, macrophages, epithelial cells, and T cells. Macrophages induce a set of mediators that are involved in asthma pathogenesis and include MIF, Prostaglandin, CXCR3L, IL-12, IL-1ß, TSLP, IL-18, IL-33, LTC4, MMP-2, TNF-α, IL-17, IL-10, TGF-ß and IL-27. While, T-cells mediators effect in asthma is induced via TNF-α, IL-17, IL-10, TGF-ß, IL-27, Tim, GM-CSF, IL-2, IL-4, IL-13, INF- γ, and PPAR γ. However, the epithelial cells induced mediators potentiate proinflammatory effects, increase the number of Th2 cells, activate dendritic cells, increase the number of mast cells, and recruit eosinophils, basophils, neutrophils, T-cells, monocytes and dendritic cells. In this review, the role of T cells, macrophages, and epithelial cells is discussed.