Environmental challenges induce asthma exacerbations that, in part, are mediated by alterations in ASM function. Allergens as well as viruses and bacterial infections are common stimuli for asthma exacerbations. Traditionally, these environmental challenges are thought to be mediated through airway inflammation and trafficking leukocytes. Contemporary thought suggests that structural cells, namely, ASM, in part may modulate inflammatory responses by altering cell adhesion molecule expression or secreting chemokines and cytokines. The paracrine and autocrine secretion of chemokines and cytokines may then also alter the responsiveness of ASM to contractile agonists and agents that promote bronchodilation. Repeated asthma exacerbations may induce chronic alterations in ASM manifested by myocyte hypertrophy and hyperplasia (modified from Tliba and Panettieri, Curr Allergy Asthma Rep 2008; 8:262-8).
Abbreviations: ASM: airway smooth muscle; CXCL8, CXCL10, CCL2: chemokines; DsRNA: double-stranded ribonucleic acid; ECM: extracellular matrix; FKN: fractalkine; ICAM-1: intercellular adhesion molecule-1; IFNγ: interferon gamma; IL-17: interleukin-17; LL-37: human cathelicidin antimicrobial peptide LL-37; LPS: lipopolysaccharide endotoxin; TNFα: tumor necrosis factor alpha; VCAM-1: vascular cellular adhesion molecule-1; VIP: vasoactive intestinal peptide