Staphylococcus aureus is a human pathogen with the potential to cause life-threatening diseases, but it can also be found as a commensal in up to 50% of the population. Its main reservoir is located in the nostrils, where macrophages are the principal mucosal APC and elicit a predominantly IL-10 response. Induction of IL-10 requires phosohoinositide 3-kinase activity, upon stimulation with S. aureus ligands through toll-like receptor 2 binding. It is hypothesized that IL-10 production by macrophages in the nasal mucosa allows S. aureus to persist in this niche as a commensal. To test this hypothesis, a cohort of S. aureus nasal carriers and non-carriers was developed and cytokine responses were compared between these groups. The data suggest that carriers may be producing more IL-10 than non-carriers, while TNF-α production remained unchanged, in response to heat-killed S. aureus. This differential IL-10 production could be a key factor behind S. aureus commensalism