Staphylococcus aureus is a gram-positive bacterium that is present in the nostrils of a quarter of the general population without causing any apparent disease. However, S. aureus can also act as a pathogen to cause severe infections. The factors determining the balance between its commensal and pathogenic states are not understood. Emerging evidence suggests that S. aureus, in addition to inducing a pro-inflammatory response, may have the capacity to modulate the host immune system. The latter is in part the result of recognition of specific molecules embedded in the peptidoglycan layer of the staphylococcal cell wall that bind to TLR2 on host antigen-presenting cells and induce a strong IL-10 response that down regulates the adaptive T cell response. This mechanism can partially explain the duality of interactions between S. aureus and the human immune system by favoring nasal colonization instead of staphylococcal diseases. In this review, we discuss the molecular and cellular basis of this mechanism and explore its clinical implications.
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