Characterizing the mechanisms by which community associated methicillin resistant Staphylococcus aureus influences keratinocyte innate immune responses during recurrent infection

摘要: Community associated–methicillin resistant Staphylococcus aureus (CA–MRSA) infection has become a major health concern. In human epidermal keratinocytes, S. is mainly recognized through toll–like receptor 2 (TLR2) and its co–receptor, CD14. We hypothesize that CA–MRSA isolates cause recurrent infections by interrupting TLR2–mediated inflammation in keratinocytes. Recurrent CA–MRSA bacterial culture supernatant exposure to keratinocytes vitro resulted in significant decreases pro anti–inflammatory cytokine HMGB1 secretion from keratinocytes as assessed by ELISAs. Recurrent CA–MRSA live infection did not result in significant changes cytokine or secretion, surface receptor expression, NFκB activation post as assessed ELISA Western blot respectively. conclude that under our experimental conditions, do suppress TLR2–mediated in keratinocytes means of cell surface virulence factors. More likely, secreted factors isolates mediate this effect, perhaps interrupting TLR2 signaling pathogen recognition the host immune system.