Contractile agonists, like methacholine, can directly activate receptors on ASM cells that initiate myocyte contraction and consequent bronchoconstriction, and this is the basis of the methacholine challenge test sometimes used to diagnose asthma. A variety of chemical and physical stimuli can trigger bronchoconstriction ( Table 1). The excessive contractile response of ASM in asthma results in inordinate bronchoconstriction and airflow obstruction in response to relatively little provocation this phenomenon is denoted as airway hyperresponsiveness. This review is meant to update practicing physicians with current knowledge about these less discussed direct effects of ASM on airway narrowing and indirect influences on airway remodeling and inflammation in asthma ( Fig. Through impaired airway relaxation and mediation of structural changes and inflammatory signaling, the ASM cell plays multiple diverse roles in the pathophysiology of asthma. Although airway smooth muscle (ASM) has been implicated in constrictor hyperresponsiveness in asthma for decades, other important roles of ASM have recently been identified. In recent years, there has been much attention on inflammation in asthma, for example, whether the type of inflammatory cell predominately found in the airway denotes a specific phenotype in asthma or whether targeting antibodies, inflammatory cytokines, and inflammatory cells is helpful for the treatment of asthma ( 56, 96, 115). Structural and inflammatory changes throughout the airway wall lead to bronchial thickening and edema as well as increased mucus production and bronchoconstriction, all of which contribute to the episodic airflow obstruction typically found in asthma ( Fig. 1 It is characterized by intermittent airflow obstruction and airway inflammation, producing symptoms of chest tightness, wheezing, and cough. Asthma is a chronic disease of the airways affecting over 24 million people in the United States ( 94).
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