Staphylococcus Research Today is a free monthly online journal that collates and summarizes the latest research about Staphylococcus, including details on mrsa, hospitals, infection, antibiotic resistance, superbugs.

The extracellular adherence protein (Eap) of Staphylococcus aureus inhibits wound healing by interfering with host defense and repair mechanisms.

Athanasopoulos AN, Economopoulou M, Orlova VV, Sobke A, Schneider D, Weber H, Augustin HG, Eming SA, Schubert U, Linn T, Nawroth PP, Hussain M, Hammes HP, Herrmann M, Preissner KT, Chavakis T

Experimental Immunology Branch, NCI, NIH, Center Dr, Rm 4B17, Bethesda, MD 20892, USA.

Staphylococcus aureus is a major human pathogen interfering with host-cell functions. Impaired wound healing is often observed in S aureus-infected wounds, yet, the underlying mechanisms are poorly defined. Here, we identify the extracellular adherence protein (Eap) of S aureus to be responsible for impaired wound healing. In a mouse wound-healing model wound closure was inhibited in the presence of wild-type S aureus and this effect was reversible when the wounds were incubated with an isogenic Eap-deficient strain. Isolated Eap also delayed wound closure. In the presence of Eap, recruitment of inflammatory cells to the wound site as well as neovascularization of the wound were prevented. In vitro, Eap significantly reduced intercellular adhesion molecule 1 (ICAM-1)-dependent leukocyte-endothelial interactions and diminished the consequent activation of the proinflammatory transcription factor nuclear factor kappaB (NFkappaB) in leukocytes associated with a decrease in expression of tissue factor. Moreover, Eap blocked alphav-integrin-mediated endothelial-cell migration and capillary tube formation, and neovascularization in matrigels in vivo. Collectively, the potent anti-inflammatory and antiangiogenic properties of Eap provide an underlying mechanism that may explain the impaired wound healing in S aureus-infected wounds. Eap may also serve as a lead compound for new anti-inflammatory and antiangiogenic therapies in several pathologies.

Published 23 March 2006 in Blood, 107(7): 2720-7.
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