• Sara H Bengtson, Stephen B Phagoo, Anna Norrby-Teglund, Lisa Påhlman, Matthias Mörgelin, Bruce L Zuraw, L M Fredrik Leeb-Lundberg, and Heiko Herwald.
• Department of Clinical Sciences, Section for Clinical and Experimental Infection Medicine, Lund University, Tornavägen 10, SE-221 84 Lund, Sweden.
• Blood. 2006 Sep 15; 108 (6): 2055-63.

AbstractAn inappropriate host response to invading bacteria is a critical parameter that often aggravates the outcome of an infection. Staphylococcus aureus is a major human Gram-positive pathogen that causes a wide array of community- and hospital-acquired diseases ranging from superficial skin infections to severe conditions such as staphylococcal toxic shock. Here we find that S aureus induces inflammatory reactions by modulating the expression and response of the B1 and B2 receptors, respectively. This process is initiated by a chain of events, involving staphylococcal-induced cytokine release from monocytes, bacteria-triggered contact activation, and conversion of bradykinin to its metabolite desArg(9)bradykinin. The data of the present study implicate an important and previously unknown role for kinin receptor regulation in S aureus infections.

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