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The Cells of Asthma

Dwaine Rieves, MD, FCCP
Author and Funding Information

Affiliations: Rockville, MD 
 ,  Dr. Rieves is Medical Officer, Center for Biologics Evaluation and Research, US Food and Drug Administration.

Correspondence to: Dwaine Rieves, MD, FCCP, FDA/CBER, 1401 Rockville Pike, HPM-57, Rockville, MD 20852-1448



Chest. 2001;119(5):1299-1300. doi:10.1378/chest.119.5.1299
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Eosinophils, lymphocytes, and mast cells are generally recognized as the central cellular orchestrators of airway inflammation within most conceptual models of asthma. Based on clinical correlates, these models may be broadly grouped into those that focus on an atopic pathogenesis or nonatopic pathogenesis of airway inflammation. Many definitions of “atopy” are utilized, but in general, the atopic models are clinically characterized by the presence of positive skin test reactions to known aeroallergens in a pattern consistent with IgE-mediated reactions. The nonatopic models lack the skin test reactivity to aeroallergens and, by implication, IgE is thought to be less important in the inflammation pathogenesis.1 To a variable extent, both models incorporate the same effector cells and the same soluble mediators. The cellular variability and overlap of the two models are exemplified by a study of atopic and nonatopic patients in which the cellular content of sputum was examined at two time points: during an asthma exacerbation and 2 weeks following treatment.2 The investigators found that the sputum content of eosinophils varied nearly 100-fold among the patients at each time point. However, all patients, including the nonatopic patients, had a decrease in the sputum content of eosinophils following corticosteroid therapy. While these observations may simply reflect a noncausal pharmacodynamic effect of the steroid therapy, another interpretation of the findings is that even “low” levels of airway mucosal eosinophilia may have clinical consequences in some patients.

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asthma

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