Abstract
While asthma is considered an inflammatory disorder of theconducting airways, it is becoming increasingly apparent thatthe disease is heterogeneous with respect to immunopathology,clinical phenotypes, response to therapies, and natural history.Once considered purely an allergic disorder dominated by Th2-type lymphocytes, IgE, mast cells, eosinophils, macrophages,and cytokines, the disease also involves local epithelial,mesenchymal, vascular and neurologic events that areinvolved in directing the Th2 phenotype to the lung andthrough aberrant injury-repair mechanisms to remodelingof the airway wall. Structural cells provide the necessary"soil" upon which the "seeds" of the inflammatory responseare able to take root and maintain a chronic phenotype andupon which are superimposed acute and subacute episodesusually driven by environmental factors such as exposure toallergens, microorganisms, pollutants or caused by inadequateantiinflammatory treatment. Greater consideration of additionalimmunologic and inflammatory pathways are revealing newways of intervening in the prevention and treatment of thedisease. Thus increased focus on environmental factors beyondallergic exposure (such as virus infection, air pollution, and diet)are identifying targets in structural as well as immune andinflammatory cells at which to direct new interventions. © 2008 Blackwell Publishing.
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Holgate, S. T. (2009). Pathogenesis of Asthma. In Allergy and Allergic Diseases, Second Edition (Vol. 2, pp. 1608–1631). Wiley-Blackwell. https://doi.org/10.1002/9781444300918.ch78
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