Abstract
Accumulating patholological and physiological evidence in the last few years suggests that the airway inflammation and remodeling that characterize asthma occur not only in the central airways but extend to the distal lung and the lung parenchyma. The distal airways are capable of producing T-helper (Th)2 cytokines as well as chemokines, and more recently, they have been recognized as a predominant site of airflow obstruction in asthmatics. A similar TH2-type cytokine profile and infiltration of inflammatory cells has also been reported in the lung parenchyma. The inflammation at this distal site has been described as more severe when compared with the large airway inflammation, and evidence of remodeling in the lung periphery is emerging. Recognition of asthma as a disease of the entire respiratory tract has an important clinical significance highlighting the need also to consider the distal lung as a target in any therapeutic strategy for effective treatment of this disease.
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More From: Seminars in Respiratory and Critical Care Medicine
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