Staphylococcus aureus internalisation enhances bacterial survival through modulation of host immune responses and mast cell activation.

Chronic rhinosinusitis (CRS) is a chronic inflammatory condition of the upper airways affecting up to 15% of the population, significantly impacting upon patients' quality of life and resultant healthcare resources.1 Whilst the pathophysiological mechanisms underlying CRS are not fully understood, I Staphylococcus aureus i ( I S aureus i ) has been shown to play a prominent role.2-4 In addition to its presence on the sinonasal mucosal surface, we previously demonstrated I S aureus i harbouring within mast cells in nasal polyps.2 We revealed that following I S aureus i intracellular uptake and proliferation, bacteria were released into the extracellular space following mast cell rupture, which potentially contributed to the repopulation of depleted surface colonies.3 Recent evidence suggests that patients with nasal polyps, and especially those with recalcitrant disease, not only have intracellular reservoirs of I S aureus i but also elevated levels of IgE specific to I S aureus i and their toxins.5 Activation of mast cells via localized anti- I S aureus i IgE would normally enable them to contribute towards clearance of some of the subepithelial bacterial colonies through phagocytosis.6 However, it is postulated that modulation of the local host immune response by I S aureus i may blunt this response, resulting in enhanced bacterial survival and persistence. Using bone-derived murine mast cells and the HMC-1 line, Abel et al showed a mast cell response to eradicate I S aureus i infection through the release of pre-formed mediators and extracellular traps.8 However, I S aureus i was able to subvert these killing mechanisms through its internalization. [Extracted from the article]