The lungs present an immunological challenge for the host as they are most frequently targeted by pathogens. Alveolar macrophages are critical to pulmonary host defence and innate immunity. In addition to improving pulmonary mechanics, its components have also been seen to modulate innate pulmonary immunity. Here, we evaluated the potential anti-inflammatory effects of three exogenous surfactants (Curosurf, Liposurf and Synsurf) on the lipopolysaccharide (LPS)-stimulated and un-stimulated rat alveolar macrophage (AM) cell line NR8383. Exogenous surfactants (Curosurf, Liposurf and Synsurf) standardised to dipalmitoylphosphatidylcholine (DPPC) content of 500-1500 μg/ml were incubated with LPS (1 μg/ml)-stimulated and un-stimulated NR8383 AMs over a 24-h exposure period. Proteomics was employed to detect protein expression. Our results showed that exogenous surfactants inhibit secretion of pro-inflammatory cytokines and influence the production of reactive oxygen species (ROS) in NR8383 AMs. In addition, the inhibitory effect of surfactants on cytokine secretion was displayed in a dose-dependent manner as well as a threshold effect was seen for all three surfactants. This may result from unique mechanisms of decreasing cell signalling or up-regulating anti-inflammatory activity that was further elucidated via proteomics. Our findings indicate that the anti-inflammatory activity of surfactant products used in the treatment of neonatal respiratory distress syndrome (nRDS) may depend upon the specific preparation or dose used. In this regard, Synsurf, a synthetic peptide containing surfactant, displayed the same “protective” nature to that of animal derived surfactant protein B/C (SP-B/C) containing surfactants.
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