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Pathogenesis of asthma

Mark Liu, MD
Section Editor
Bruce S Bochner, MD
Deputy Editor
Helen Hollingsworth, MD


The "classic" signs and symptoms of asthma are intermittent dyspnea, cough, and wheezing. This well-recognized syndrome is characterized by variable airflow limitation and by airway hyperresponsiveness, which represents an exaggerated contractile response of the airways to a variety of stimuli.

Atopy, or the genetic predisposition to develop specific IgE antibodies directed against common environmental allergens, is the strongest identifiable risk factor for the development of asthma [1]. While the association of asthma and atopy is undisputed, the pathways by which atopy is expressed as clinical asthma and by which asthma occurs in the absence of atopy are not as clearly defined [1]. Intrinsic abnormalities in airway smooth muscle function, airway remodeling in response to injury or inflammation, and interactions between epithelial and mesenchymal cells appear to modulate and add to the effects of airway inflammation in creating the clinical presentation of asthma. Different phenotypes of asthma that can be defined clinically reinforce the notion that asthma is really a syndrome with multiple underlying mechanisms [2].

The inflammatory, physiologic, and structural factors that contribute to the pathogenesis of asthma will be reviewed here, focusing on aspects that aid in the understanding of the clinical presentation of asthma and its treatment.

Discussions of the genetics, clinical risk factors (eg, atopy, allergen exposure, viral illness, gender, and smoking), diagnosis, and management of asthma are provided separately. (See "Genetics of asthma" and "Risk factors for asthma" and "Diagnosis of asthma in adolescents and adults" and "Asthma in children younger than 12 years: Initial evaluation and diagnosis".)


Airway biopsies obtained by bronchoscopy have demonstrated that inflammation in asthma generally involves the same cells that play prominent roles in the allergic response in the nasal passages and skin, whether the individual is atopic or not. This supports the belief that the consequences of mast cell activation, mediated by a variety of cells, cytokines, and other mediators, are key to the development of clinical asthma. (See "Pathogenesis of allergic rhinitis (rhinosinusitis)".)


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Literature review current through: Dec 2014. | This topic last updated: May 16, 2014.
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