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Resume La BPCO sera durant la prochaine decennie la troisieme cause de mortalite dans le monde. Due principalement au tabagisme a la cigarette, elle revet une gravite distincte selon les individus, impliquant des facteurs environnementaux et genetiques incompletement apprehendes. Des travaux recents mettent en cause la colonisation microbienne des bronches et les exacerbations infectieuses comme facteur d'aggravation via l'effet pro-inflammatoire et le stress oxydatif. Cela implique de recenser les moyens d'une prevention anti-infectieuse au nombre desquels la place de l'antibiotherapie prophylactique et des antioxydants doit etre discutee.

The tachykinin substance P (SP) is present in lung sensory nerve endings and may be released after neurogenic stimulation. Its role in the pathogenesis of asthma is still unclear. Nevertheless, it may play a major role in airway neurogenic inflammation. Alveolar macrophages are the predominant cells of the airway space and are involved in various types of airway inflammation. We studied guinea pig alveolar macrophage response to SP and other related peptide (C- and N-terminal sequences, NK1-receptor agonist) stimulation. Alveolar guinea pig macrophages were recovered by bronchoalveolar lavage (BAL). Macrophage reactive oxygen intermediate (ROI) production was studied by luminol-dependent chemiluminescence with several concentrations of SP and related peptides. Eicosanoid synthesis after stimulation was evaluated by thin-layer chromatography (TLC) and enzyme-linked immunosorbent assay (ELISA). SP, C-terminal sequence, and NK1-receptor agonist significantly increased ROI production by alveolar macrophages (P < 0.01). NK1-agonist and C-terminal sequence modified arachidonic acid metabolism and induced a significant increase in prostaglandin (PG)D2 synthesis (211% and 66%, respectively). We concluded that SP and related peptides directly affect guinea pig alveolar macrophages by inducing the production of inflammatory metabolites.