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Am J Physiol Lung Cell Mol Physiol (April 26, 2002). doi:10.1152/ajplung.00062.2002
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Articles in PresS, published online ahead of print April 26, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00062.2002
Submitted on February 19, 2002
Accepted on April 23, 2002

The late asthmatic response is linked with increased surface tension and reduced surfactant protein (SP)-B in mice

Angela Haczku*, Elena N. Atochina, Yaniv Tomer, Yang Cao, Colleen Campbell, Seth T. Scanlon, Scott J. Russo, Goran Enhorning, and Michael F. Beers

* To whom correspondence should be addressed. E-mail: haczku{at}mail.med.upenn.edu.

Pulmonary surfactant dysfunction may significantly contribute to small airway obstruction during the asthmatic response but neither its exact role nor its regulation is clear. Surfactant function and composition was studied in an Aspergillus fumigatus (Af)-induced late phase allergic airway response in sensitized BALB/c mice. The peak of Af-induced airway hyperresponsiveness in sensitized and challenged mice 24h after allergen provocation coincided with a significant fall in surface activity of the pulmonary surfactant. The underlying changes included time dependent elaboration of eotaxin and IL-5 followed by eosinophil influx into the airways. The height of airway inflammation and hyperresponsiveness was preceded by release of IL-4 and marked reductions in SP-B, a hydrophobic surfactant protein responsible for maintaining low surface tension of the lining fluid of distal airspaces. Further, intratracheal administration of IL-4 significantly inhibited SP-B indicating a regulatory role of this cytokine in the surfactant biophysical changes. Thus, surfactant dysfunction induced by an IL-4-driven SP-B deficiency after allergen provocation may be an important part of the late asthmatic airway response.




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