Effect Of Lung Surfactant Research Articles

Interaction between lung surfactant and nitric oxide production by alveolar macrophages stimulated by group B streptococci.

The major etiologic agent in neonatal pneumonia and meningitis is group B streptococci (GBS). Nitric oxide (NO) production by alveolar macrophages (AM) in response to Gram-positive bacteria such as GBS and the effect of surfactant on this production have received little attention. We studied production of NO by GBS-stimulated AM using the Griess reaction, the effect of lung surfactant on this NO production, and the possible lipid peroxidation (LPO) of surfactant caused by NO. The LPO test was used to measure surfactant peroxidation. Heat-killed and live GBS were found to stimulate NO production by rat alveolar macrophages, and the presence of interferon gamma (IFN-gamma) increased this stimulation in a synergistic manner. Curosurf(R), the natural surfactant used in our study, significantly reduced NO production in various sets of experiments. Lipid peroxidation of surfactant was noted when NO was produced by stimulated AM, a phenomenon that could be suppressed by NG-monomethyl L-arginine (L-NMMA), the inhibitor of NO synthase. In the lung of GBS-infected neonates, nitric oxide produced by AM might contribute to the destruction of surfactant caused by inflammatory cells. Pediatr Pulmonol. 2000; 30:106- 113.

In vitro effect of lung surfactant on alveolar macrophage defence mechanisms against Cryptococcus neoformans.

The effects of a modified natural porcine surfactant (Curosurf) on phagocytosis and killing of Cryptococcus neoformans by alveolar macrophages and on the production of superoxide anions were investigated in vitro. Attachment and ingestion were evaluated separately by a fluorescent quenching technique. The nitroblue tetrazolium reduction test was used as an indirect measurement of superoxide anion production. Killing was assessed by a colony-forming assay. Surfactant induced increased ingestion of C. neoformans, unopsonized as well as opsonized with fresh serum or anticryptococcal polyclonal IgG. Surfactant had, however, no effect on the attachment or killing of unopsonized or opsonized C. neoformans by the alveolar macrophages. In addition, the enhancement of the oxidative metabolism of the macrophages after stimulation with opsonized yeast was impaired, although the killing was not affected. This study indicates that in vitro Curosurf can influence the alveolar macrophage defence against C. neoformans by enhancing its ingestion and by interacting with the superoxide anions release from alveolar macrophages stimulated with fresh serum or anticryptococcal polyclonal IgG opsonized yeast cells.