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Following tissue/vascular injury, several defense mechanisms including the innate immune system, wound repair and inflammatory responses are orchestrated to ensure proper wound healing. Starting with non-healing wounds, the intravascular manifestation of microbial infections, particularly Staphylococcus aureus infection, is often associated with a severe, and sometimes catastrophic disease. Many host factors contribute to vascular/endothelial tropism of S. aureus including extracellular matrix proteins, endothelial cell receptors, and platelets that are engaged together with S. aureus cell wall adhesins. Recently, the role of secreted staphylococcal factors that were initially identified by virtue of their binding function with host proteins and ligands has been reappraised in this regard. Among these structurally non-related proteins, coagulase (Coa), the extracellular fibrinogen binding protein (Efb), the extracellular matrix binding protein (Emp), or the extracellular adhesive protein (Eap), are the most prominent ones to be associated with an endovascular disease. Newly discovered interactions with host components may account for profound effects of these proteins on immunmodulation and impairement of wound healing. Here, the anti-inflammatory and anti-angiogenic properties of S. aureus Eap will be further detailed, based on novel in vivo and in vitro results. These new functions of Eap characterize the bacterial protein as a good target candidate for improving repair of infected and/or non-healing wounds. Likewise, Eap may serve as lead structure for the development of new treatment modalities for the inhibition of (tumor-)angiogenesis and hyper-inflammation.
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J. Vasc. Biol. 42, Sup:2 (2005) p5