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Am J Physiol Lung Cell Mol Physiol (December 21, 2001). doi:10.1152/ajplung.00213.2001
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Articles in PresS, published online ahead of print December 20, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00213.2001
Submitted on June 8, 2001
Accepted on December 31, 1969

Diesel Particles Increase Phosphatidyl Choline ReleaseThrough a NO Pathway in Alveolar Type 2 Cells

Philippe Juvin1*, Thierry Fournier2, Martine Grandsaigne1, Jean-Marie Desmonts1, and Michel Aubier1

1 408, INSERM, PARIS, France
2 427, INSERM, PARIS, France

* To whom correspondence should be addressed. E-mail: pjuvin{at}free.fr.

Diesel exhaust particles (DEPs) have been shown to affect in vivo as well as in vitro the respiratory function and in particular the immune response to infection and allergens. In the current study, we investigated the effect of DEPs on the production of phosphatidyl choline (PC) - a major constituent of surfactant - by rat alveolar type 2 (AT2) primary cells in vitro. Our results demonstrate that incubation of AT2 cells with DEPs lead to a time- and dose-dependent increase in labeled PC release. This effect was mimicked by NO donors, cGMP and abolished by inhibitors of NO synthase. In addition, NO synthase inhibitor inhibits by itself the basal secretion of PC. We next examined the effects of DEPs on NO synthase gene expression and showed that DEPs increase NO production and up regulate both protein content and mRNA levels of the inducible NO synthase (NOS II). Together our data demonstrate that DEPs alter the production of surfactant by AT2 cells through a NO dependent signaling pathway.




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