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Am J Physiol Lung Cell Mol Physiol 282: L1075-L1081, 2002. First published December 21, 2001; doi:10.1152/ajplung.00213.2001
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Vol. 282, Issue 5, L1075-L1081, May 2002

Diesel particles increase phosphatidylcholine release through a NO pathway in alveolar type II cells

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

1 Unité 408, Institut National de la Santé et de la Recherche Médicale, 75870 Paris Cedex 18; and 2 Unité 427, Institut National de la Santé et de la Recherche Médicale, Faculté des Sciences Pharmaceutiques et Biologiques, Université René Descartes Paris 5, 75006 Paris, France

Diesel exhaust particles (DEPs) have been shown in vivo as well as in vitro to affect 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 phosphatidylcholine (PC), a major constituent of surfactant, by rat alveolar type II (ATII) primary cells in vitro. Our results demonstrate that incubation of ATII cells with DEPs lead to a time- and dose-dependent increase in labeled PC release. This effect was mimicked by nitric oxide (NO) donors and cGMP and was abolished by inhibitors of NO synthase (NOS). In addition, a NOS inhibitor inhibits by itself the basal secretion of PC. We next examined the effects of DEPs on NOS gene expression and showed that DEPs increase NO production and upregulate both protein content and mRNA levels of the inducible NOS (NOS II). Together our data demonstrate that DEPs alter the production of surfactant by ATII cells through a NO-dependent signaling pathway.

surfactant; nitric oxide

* P. Juvin and T. Fournier contributed equally to this work.




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