Date of Award

2014

Degree Type

Thesis

Degree Name

Master of Science (MS)

Department

Biological Science

Abstract

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

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.

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