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Innate Immune Responses and Chronic Obstructive Pulmonary Disease

"Terminator" or "Terminator 2"?

Division of Allergy-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois

Correspondence and requests for reprints should be addressed to Robert P. Schleimer, Ph.D., Northwestern University Feinberg School of Medicine, Division of Allergy-Immunology, 240 East Huron, Room 2318, Chicago, IL 60611. E-mail: rpschleimer{at}northwestern.edu

Innate immune responses appear to be partially responsible for maintaining inflammation and tissue destruction in chronic obstructive pulmonary disease. In the early stages of the disease in smokers, the airways are bombarded with large quantities of particulate material, and activation of phagocytic cells results in the release of many of the mediators believed to remodel the airways. Ironically, failure of the innate immune defense system, either by inherited deficiency or as a result of chronic smoke inhalation, is likely to result in increased susceptibility to infectious disease and exacerbations of chronic obstructive pulmonary disease. It is well known that deficiencies in the production of collectins, pentraxins, and complement can lead to increased infections, and several studies indicate that deficiency in one or another innate defense component is associated with increased exacerbations. Corticosteroids reduce exacerbations in part because of their ability to boost the production of innate host-defense molecules. Therapeutic approaches that stimulate the generation of antimicrobial molecules in the lungs might be able to reduce disease exacerbations.

Key Words: acute phase responses • corticosteroids • exacerbations • inflammation • opsonins

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