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J Appl Physiol 95: 844-853, 2003; doi:10.1152/japplphysiol.00192.2003
8750-7587/03 $5.00
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HIGHLIGHTED TOPICS
Airway Hyperresponsiveness: From Molecules to Bedside

Invited Review: Do inflammatory mediators influence the contribution of airway smooth muscle contraction to airway hyperresponsiveness in asthma?

Darren J. Fernandes,1,2 Richard W. Mitchell,1 Oren Lakser,3,4 Maria Dowell,1,3 Alastair G. Stewart,2 and Julian Solway1

1Section of Pulmonary and Critical Care Medicine, University of Chicago, and 3Children's Memorial Hospital and 4Northwestern University, Chicago, Illinois 60637; and 2Department of Pharmacology, University of Melbourne, Melbourne, Victoria 3010, Australia

It is now accepted that a host of cytokines, chemokines, growth factors, and other inflammatory mediators contributes to the development of nonspecific airway hyperresponsiveness in asthma. Yet, relatively little is known about how inflammatory mediators might promote airway structural remodeling or about the molecular mechanisms by which they might exaggerate smooth muscle shortening as observed in asthmatic airways. Taking a deep inspiration, which provides relief of bronchodilation in normal subjects, is less effective in asthmatic subjects, and some have speculated that this deficiency stems directly from an abnormality of airway smooth muscle and results in airway hyperresponsiveness to constrictor agonists. Here, we consider some of the mechanisms by which inflammatory mediators might acutely or chronically induce changes in the contractile apparatus that in turn might contribute to hyperresponsive airways in asthma.

actin; myosin; airflow obstruction


Address for reprint requests and other correspondence: J. Solway, Section of Pulmonary and Critical Care Medicine, Univ. of Chicago, 5841 S. Maryland Ave., MC6026, Chicago, IL 60637 (E-mail: jsolway{at}medicine.bsd.uchicago.edu).




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