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. Author manuscript; available in PMC: 2009 Nov 30.
Published in final edited form as: Respir Physiol Neurobiol. 2008 Jul 31;163(1-3):166–177. doi: 10.1016/j.resp.2008.07.020

Figure 1. Airway wall remodeling in asthma.

Figure 1

In asthma, the inflammatory response is marked by increased production of Th2 cytokines such as interleukin-4 (IL-4), IL-5, IL-9 and IL-13, by CD4+ lymphocytes (T-cells) and immunoglobulin E overproduction by CD20+ lymphocytes (B-cells). These mediators of inflammation recruit inflammatory cells, such as eosinophils, that release proteins, such as major basic protein (MBP) and eosinophil cationic protein (ECP), which directly injure the respiratory epithelial cells and may lead to epithelial sloughing. Inflammatory mediators also induce the expression of the inducible nitric oxide synthase (iNOS). Increased NO has been shown to produce cytotoxic effects on respiratory epithelial cells, attributed to the formation peroxynitrite (ONOO−), a highly reactive intermediate generated by a reaction of NO and superoxide anions (O2−). A portion of the NO produced by the epithelium can escape by diffusion to the gas phase and appear in the exhaled breath. Damaged epithelial cells release transforming growth factor β (TGF-β), which is associated with increased collagen production by fibroblasts within the extracellular matrix.