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Physiological Reviews, Vol. 82, No. 1, January 2002, pp. 19-46; 10.1152/physrev.00020.2001.
Copyright ©2002 by the American Physiological Society
Departments of Medicine and Cell Biology/Physiology, Washington University School of Medicine, St. Louis, Missouri
Holtzman, Michael J.,
Jeffrey D. Morton,
Laurie P. Shornick,
Jeffrey W. Tyner,
Mary P. O'Sullivan,
Aurita Antao,
Mindy Lo,
Mario Castro, and
Michael J. Walter.
Immunity, Inflammation, and Remodeling in the
Airway Epithelial Barrier: Epithelial-Viral-Allergic
Paradigm. Physiol. Rev. 82: 19-46, 2002.
The concept that airway inflammation leads
to airway disease has led to a widening search for the types of
cellular and molecular interactions responsible for linking the initial
stimulus to the final abnormality in airway function. It has not yet
been possible to integrate all of this information into a single model
for the development of airway inflammation and remodeling, but a useful framework has been based on the behavior of the adaptive immune system.
In that paradigm, an exaggeration of T-helper type 2 (Th2) over Th1
responses to allergic and nonallergic stimuli leads to airway
inflammatory disease, especially asthma. In this review, we summarize
alternative evidence that the innate immune system, typified by actions
of airway epithelial cells and macrophages, may also be specially
programmed for antiviral defense and abnormally programmed in
inflammatory disease. Furthermore, this abnormality may be inducible by
paramyxoviral infection and, in the proper genetic background, may
persist indefinitely. Taken together, we propose a new model that
highlights specific interactions between epithelial, viral, and
allergic components and so better explains the basis for airway
immunity, inflammation, and remodeling in response to viral infection
and the development of long-term disease phenotypes typical of
asthma and other hypersecretory airway diseases.
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