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.
Keywords:
Asthma, epithelial cell, macrophage, T cell, Type 2 inflammation, cytokines, pathogenesis
Graphical Abstract
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