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Published ahead of print on June 5, 2003, doi:10.1164/rccm.200211-1262OC
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American Journal of Respiratory and Critical Care Medicine Vol 168. pp. 342-347, (2003)
© 2003 American Thoracic Society

Prenatal Cigarette Smoke Decreases Lung cAMP and Increases Airway Hyperresponsiveness

Shashi P. Singh, Edward G. Barrett, Roma Kalra, Seddigheh Razani-Boroujerdi, Raymond J. Langley, Viswanath Kurup, Yohannes Tesfaigzi and Mohan L. Sopori

Respiratory Immunology and Asthma Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico; and VA Medical Center and Medical College of Wisconsin, Milwaukee, Wisconsin

Correspondence and requests for reprints should be addressed to Mohan L. Sopori, Ph.D., Respiratory and Immunology Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive SE, Albuquerque, NM 87108. E-mail: msopori{at}lrri.org

Epidemiologic studies suggest that in utero exposure to tobacco smoke, primarily through maternal smoking, increases the risk for asthma in children; however, the mechanism of this phenomenon is not clear. Cyclic adenosine monophosphate relaxes airway smooth muscles in the lung and acts as an antiasthmatic. In this study, we examined the effects of in utero cigarette smoke exposure of Balb/c mice on airway responsiveness, as determined by Penh measurements. Animals exposed prenatally but not postnatally to cigarette smoke exhibited increased airway hyperresponsiveness after a single intratracheal injection of Aspergillus fumigatus extract. The increased airway hyperresponsiveness was not associated with increased leukocyte migration or mucous production in the lung but was causally related to decreased lung cyclic adenosine monophosphate levels, increased phosphodiesterase-4 enzymatic activity, and phosphodiesterase-4D (PDE4D) isoform-specific messenger ribonucleic acid expression in the lung. Exposure of adult mice to cigarette smoke did not significantly alter airway responsiveness, cyclic adenosine monophosphate levels, or the phosphodiesterase activity. These results suggest that prenatal exposure to cigarette smoke affects lung airway reactivity by modulating the lung cyclic adenosine monophosphate levels through changes in phosphodiesterase-4D activity, and these effects are independent of significant mucous production or leukocyte recruitment into the lung.

Key Words: asthma • phosphodiesterase-4D • Aspergillus fumigatus • airway responsiveness




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