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Published ahead of print on June 5, 2003, doi:10.1164/rccm.200211-1262OC

Am. J. Respir. Crit. Care Med., Volume 168, Number 3, August 2003, 342-347

A more recent version of this article appeared on August 1, 2003
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Submitted on November 11, 2002
Accepted on May 29, 2003

Prenatal cigarette smoke decreases lung cAMP and increases airway hyperresponsiveness

Shashi P Singh1, Edward G Barrett1, Roma Kalra1, Seddigheh Razani-Boroujerdi1, Raymond J Langley1, Viswanath Kurup2, Yohannes Tesfaigzi1, and Mohan L Sopori1*

1 Respiratory Immunology and Asthma Program, Lovelace Respiratory Research Institute, Albuquerque, NM, USA, 2 Allergy, VA Medical Center, Milwaukee, WI, USA; Pediatrics and Medicine, Medical College of Wisconsin, Milwaukee, WI, USA

* To whom correspondence should be addressed. E-mail: msopori{at}lrri.org.

Epidemiological 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 anti-asthmatic. 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 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: in utero exposure, tobacco smoke, Aspergillus fumigatus antigen, asthma, phosphodiesterase-4D




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