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Peribronchial inflammation (1–3) and exaggerated bronchospastic responses to antigen-specific and nonspecific stimuli (airways hyperresponsiveness [AHR]) are the pathologic and physiologic cornerstones of the asthmatic syndrome. Eosinophils are believed to play an important role in these responses, as tissue eosinophilia is a common feature in asthmatic airways, and eosinophils have been demonstrated to cause mucosal injury and likely contribute to the generation of altered lung physiology. The initiation and maintenance of allergic airway inflammation is mediated by poorly defined mechanisms. Even more confounding is the appreciation that different immunologic processes mediate different facets of asthma and that various types of inflammatory responses differentially contribute to the multiple features manifested by asthmatic patients. This is reflected in studies that suggest that, in addition to eosinophils, other cells — including mast cells, lymphocytes, and neutrophils — contribute to asthma pathogenesis (4–6). As a result, it has been difficult to design specific, inflammation-based therapeutic interventions for this disorder. Recent studies, however, have added to our understanding of the role of chemokines and chemokine receptors in the generation of eosinophilic and noneosinophilic airway inflammatory responses. This has begun to provide an appreciation of the complex levels of organization of airway inflammatory responses, and may help to identify novel therapeutic options.

Chemokines and asthma: redundancy of function or a coordinated effort?