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*
Unité de Pharmacologie Cellulaire, Unité Associée Institut Pasteur/Institut National de la Santé et de la Recherche Médicale, Paris, France;
Department of Cell Biology, Faculty of Medicine, Vrije Universiteit, Amsterdam, The Netherlands;
Unité d’Immunophysiologie et Parasitisme Intracellulaire, Institut Pasteur, Paris, France; and
Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Cincinnati, Cincinnati OH 45267
Upon LPS exposure, mononuclear phagocytes produce TNF-
and
IL-10, two cytokines with pro- and anti-inflammatory activities,
respectively. We previously described that murine resident alveolar
macrophages, which play a central role in the immunosurveillance of the
lung alveoli, do not synthesize IL-10 in vivo or in vitro when exposed
to LPS. In the present report we demonstrate that during lung
inflammation induced by the intranasal administration of LPS,
bronchoalveolar cells collected between days 3 and 5 are able to
synthesize IL-10 when exposed to LPS. We also show that depletion of
resident alveolar macrophages by an intratracheal instillation of
liposome-encapsulated clodronate is followed by subsequent
replenishment of the airspaces by mononuclear phagocytes. This is
accompanied by the transient competence of cells for IL-10 production.
The cell capacity to produce IL-10 is evident up to 3 days and then
decreases. This led us to hypothesize that the alveolar environment
contains a down-regulator of LPS-induced IL-10 synthesis by recently
emigrating mononuclear phagocytes. We show that the surfactant protein
A, an airspace protein that has known immunomodulatory activities,
dramatically inhibits LPS-induced IL-10 formation by bone
marrow-derived macrophages. These data show a difference between
resident and inflammatory macrophages with respect to IL-10 synthesis.
Moreover, this study highlights for the first time the inhibitory role
of surfactant protein A in the anti-inflammatory activity of
macrophages through inhibition of IL-10
production.
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