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Contribution of the Distal Lung to the Pathologic and Physiologic Changes in Asthma*: Potential Therapeutic Target Roger S. Mitchell Lecture

Meri K. Tulić, PhD; Qutayba Hamid, MD
Author and Funding Information

*From the Meakins-Christie Laboratories, McGill University, Montreal, PQ, Canada.

Correspondence to: Qutayba Hamid, MD, PhD, Professor of Medicine, Meakins-Christie Laboratories, McGill University, 3626 St. Urbain St, Montreal, PQ, Canada H2X 2P2; e-mail: qutayba.hamid@mcgill.ca



Chest. 2003;123(3_suppl):348S-355S. doi:10.1378/chest.123.3_suppl.348S
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Pathologic and physiologic evidence has emerged in the last few years suggesting 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) type 2 cytokines and chemokines, and, more recently, they have been recognized as a predominant site of airflow obstruction in asthmatic patients. In the lung parenchyma, a similar Th2 cytokine profile and infiltration of inflammatory cells also has been reported. The inflammation at this distal site has been described as being more severe when compared to the large amount of airway inflammation, and evidence of remodeling in the lung periphery is emerging. The recognition of asthma as a disease of the entire respiratory tract has an important clinical significance highlighting the need to also consider the distal lung as a target in any therapeutic strategy for effective treatment of this disease.

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lung ; asthma

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