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...

Interested in reading more?

Become a Member of

Receive full access to more than 35 years of archives, as well as TS Digest, digital editions of The Scientist, feature stories, and much more!
Already a member?