Abstract
Staphylococcus aureus is a human bacterial pathogen, known to cause a variety of illnesses and infections in the hospital and community settings. It produces a large number of virulence factors used for host invasion, tissue colonization and destruction, leading to severe infections in both healthy and immunodeficient people around the world. In this paper, we studied the potential mechanisms related to methicillin resistant S. aureus (MRSA) infection, analyzed the significance of oxidative stress for survival of S. aureus, and re-identified the molecular structure, regulatory boxes, and regulons of PerR (peroxide responsive repressor) gene, a key modulator responsible for MRSA. Then, we further investigated how PerR functions in response to oxidative stress and how the PerR regulon affects S. aureus virulence. As a conclusion, we postulate that the regulation of PerR and its regulon indirectly influences the expression of virulence factors by prolonging the pathogen’s survival under harsh conditions that may lead to the increased risk of S. aureus transmission, infection, and spread of the disease.
Implication for health policy/practice/research/medical education:
Infections caused by methicillin resistant Staphylocococcus aureus (MRSA) in medical settings are common. In the 1990's, there has been an increase in skin and soft tissue infections due to MRSA strains originating from outside of the medical environment. These infections have been shown to occur mostly in healthy, young individuals. Due to the rise of MRSA, it is necessary to identify new therapeutic solutions to eradicate the pathogen and investigating unique metabolic pathways in the pathogen shows promise in potentially identifying new drug targets.
Please cite this paper as:
Ikawa Wakabayashi JY, Cheng DW. PerR-Mediated Oxidative Stress Response in Staphylococcus aureus. Jundishapur J Microbiol. 2012;5(3):443-9. DOI: 10.5812/jjm.2460
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