Immunomodulation by exogenous surfactant: effect on TNF-alpha secretion and luminol-enhanced chemiluminescence activity by murine macrophages stimulated with group B streptococci

Group B streptococci (GBS) are important pathogens in neonatal sepsis and p neumonia. GBS stimulate alveolar macrophages to produce inflammatory cytoki nes and free oxygen radicals, which can damage the lungs. In several studie s, use of exogenous surfactant in term babies has improved outcome related to sepsis and respiratory failure. The role(s) of exogenous surfactant in m odulating the inflammatory response produced by this microbe was examined. Tumor necrosis factor alpha (TNF-alpha) production and luminol-enhanced che miluminescence (LCL), a measure of respiratory burst, were investigated. Fo r measuring TNF-alpha release, RAW 264.7 murine macrophages were pre-incuba ted with bovine surfactant and stimulated with either lipopolysaccharide, l ive or heat-killed GBS type Ia. LCL was measured after macrophages were pre -incubated with or without surfactant overnight, then stimulated with GBS o r phorbol myristate acetate. Lipopolysaccharide and GBS stimulated TNF-alph a secretion from macrophages that was suppressed by exogenous surfactant in a dose-dependent fashion. GBS and phorbol myristate acetate also increased LCL from macrophages, which was significantly suppressed by pre-incubation of macrophages with exogenous surfactant. We conclude that GBS type Ia sti mulates TNF-alpha release and LCL from RAW 264.7 cells and that these respo nses are suppressed by surfactant. Suppression of inflammatory mediators by exogenous surfactant might improve respiratory disease associated with GBS , (C) 2001 Editions scientifiques et medicales Elsevier SAS.