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Staphylococcus aureus is a frequent colonizer of human skin and mucous membranes, but its interaction with the host's anti-inflammatory mechanisms has been unclear. In 24 June advanced online Nature Medicine, Triantafyllos Chavakis and colleagues at Justus-Liebig-Universität, Giessen, Germany, show that Staphylococcus aureus extracellular adherence protein (Eap) is an anti-inflammatory factor that inhibits the recruitment of host leukocytes (Nat Med 2002, DOI:10.1038/nm728).
Using an in vitro system Chavakis et al. observed that Eap disrupted β2-integrin and urokinase receptor–mediated leukocyte adhesion. In addition, in a murine model, they observed that Eap-expressing S. aureus induced a lower neutrophil recruitment in bacterial peritonitis compared to an Eap-negative strain. Isolated Eap also prevented β2-integrin-dependent neutrophil recruitment in a murine model of acute thioglycollate-induced peritonitis.
"This effect of Eap defines an entirely novel mechanism of S. aureus for resistance against the first-line host-defense mechanism, leukocyte-mediated bacterial killing," suggest the authors.
"Due to the lack of influence on the course of infection, isolated Eap could be used as a lead substance in designing new peptides or non-peptidic molecules that could serve as anti-inflammatory drugs without the possible side effect of promoting S. aureus infection," they conclude.
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