MRSA Research - Methicillin-Resistant Staphylococcus Aureus, Hospitals, Infection, Antibiotic Resistance, Superbugs

MRSA Research Today is a free monthly online journal that collates and summarizes the latest research about MRSA, including details on methicillin-resistant staphylococcus aureus, hospitals, infection, antibiotic resistance, superbugs.


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The antimicrobial peptide-sensing system aps of Staphylococcus aureus.

Li M, Cha DJ, Lai Y, Villaruz AE, Sturdevant DE, Otto M

Laboratory of Human Bacterial Pathogenesis, Genomics Unit, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, The National Institutes of Health, Hamilton, Montana, USA.

Staphylococcus aureus is a leading cause of hospital-associated and, more recently, community-associated infections caused by highly virulent methicillin-resistant strains (CA-MRSA). S. aureus survival in the human host is largely defined by the ability to evade attacks by antimicrobial peptides (AMPs) and other mechanisms of innate host defence. Here we show that AMPs induce resistance mechanisms in CA-MRSA via the aps AMP sensor/regulator system, including (i) the d-alanylation of teichoic acids, (ii) the incorporation of lysyl-phosphatidylglycerol in the bacterial membrane and a concomitant increase in lysine biosynthesis, and (iii) putative AMP transport systems such as the vraFG transporter, for which we demonstrate a function in AMP resistance. In contrast to the aps system of S. epidermidis, induction of the aps response in S. aureus was AMP-selective due to structural differences in the AMP binding loop of the ApsS sensor protein. Finally, using a murine infection model, we demonstrate the importance of the aps regulatory system in S. aureus infection. This study shows that while significant interspecies differences exist in the AMP-aps interaction, the AMP sensor system aps is functional and efficient in promoting resistance to a variety of AMPs in a clinically relevant strain of the important human pathogen S. aureus.

Published 16 November 2007 in Mol Microbiol, 66(5): 1136-47.
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