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The staphylococcus aureus surface protein IsdA mediates resistance to the innate defenses of human skin

Clarke, S.R. , Mohamed, R. , Bian, L. , Routh, A.F. , Kokai-Kun, J.F. , Mond, J.J. , Tarkowski, A. and Foster, S.J. (2007) The staphylococcus aureus surface protein IsdA mediates resistance to the innate defenses of human skin. Cell Host and Microbe, 1 (3). pp. 192-212. ISSN 1931-3128

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To link to this item DOI: 10.1016/j.chom.2007.04.005


Resistance to human skin innate defenses is crucial for survival and carriage of Staphylococcus aureus, a common cutaneous pathogen and nasal colonizer. Free fatty acids extracted from human skin sebum possess potent antimicrobial activity against S. aureus. The mechanisms by which S. aureus overcomes this host defense during colonization remain unknown. Here, we show that S. aureus IsdA, a surface protein produced in response to the host, decreases bacterial cellular hydrophobicity rendering them resistant to bactericidal human skin fatty acids and peptides. IsdA is required for survival of S. aureus on live human skin. Reciprocally, skin fatty acids prevent the production of virulence determinants and the induction of antibiotic resistance in S. aureus and other Gram-positive pathogens. A purified human skin fatty acid was effective in treating systemic and topical infections of S. aureus suggesting that our natural defense mechanisms can be exploited to combat drug-resistant pathogens.

Item Type:Article
Divisions:Life Sciences > School of Biological Sciences
Interdisciplinary centres and themes > Institute for Cardiovascular and Metabolic Research (ICMR)
ID Code:9966
Uncontrolled Keywords:MICROBIO, HUMDISEASE
Additional Information:Summary: IsdA is a surface protein expressed in vivo and decreases bacterial hydrophobicity rendering them resistant to the actions of host antimicrobials. In this manuscript, IsdA was the first S. aureus component shown to be involved in colonisation of a live human model.

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