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Unité de Défense Innée et Inflammation, Unité Associée Pasteur/Institut National de la Santé et de la Recherche Médicale U485, Institut Pasteur, 75015 Paris, France
We previously showed that the seminatural
surfactant Curosurf inhibits the in vitro synthesis of secretory type
IIA phospholipase A2 (sPLA2-IIA) in alveolar
macrophages (AM). These cells are the main source of
sPLA2-IIA in a guinea pig model of lipopolysaccharide (LPS)-induced acute lung injury (ALI). Here, we investigate the effect
of Curosurf on the pulmonary synthesis of sPLA2-IIA in this
ALI model. Our results showed that intratracheal administration of LPS
(330 µg/kg) induced an increase in pulmonary expression of
sPLA2-IIA, which was inhibited when animals received
Curosurf (16 mg/guinea pig) 30 min or 8 h after LPS instillation.
When AM were isolated from LPS-treated animals and cultured in
conditioned medium, they expressed higher levels of
sPLA2-IIA than AM from saline-treated animals. This ex vivo
sPLA2-IIA expression was significantly reduced when guinea
pigs received Curosurf 30 min after LPS instillation. Finally, we
examined the effect of Curosurf on pulmonary inflammation measured 8 or
24 h after LPS administration. Curosurf instillation 30 min or
8 h after LPS reversed the increase in tumor necrosis factor-
expression, polymorphonuclear cell extravasation, and protein
concentration in bronchoalveolar lavage fluids. Curosurf also decreased
the bronchial reactivity induced by LPS. We conclude that Curosurf
inhibits the pulmonary expression of sPLA2-IIA and exhibits
palliative anti-inflammatory effects in an animal model of ALI.
phospholipase A2; alveolar macrophage; lipopolysaccharide
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