products subvert the -induced inflammatory response in airway epithelial cells.

Chronic pulmonary infection is associated with colonization with multiple micro-organisms but host-microbe and microbe-microbe interactions are poorly understood. This study aims to investigate the differences in host responses to mono- and co-infection with and in human airway epithelial cells. We assessed the effect of co-infection with and on host signalling and inflammatory responses in the human airway epithelial cell line 16HBE, using ELISA and western blot analysis. The results show that activates MAPK and NF-κB signalling pathways, subsequently eliciting robust interleukin (IL)-8 production. However, when airway epithelial cells were co-treated with live bacteria and supernatants (conditioned medium), the pro-inflammatory response was attenuated. This anti-inflammatory effect was widely exhibited in the isolates tested and was mediated via reduced MAPK and NF-κB signalling, but not via IL-1 receptor or tumour necrosis factor receptor modulation. The staphylococcal effectors were characterized as small, heat-stable, non-proteinaceous and not cell wall-related factors. This study demonstrates for the first time the host response in a / co-infection model and provides insight into a staphylococcal immune evasion mechanism, as well as a therapeutic intervention for excessive inflammation.