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Blood, 15 September 2006, Vol. 108, No. 6, pp. 2055-2063.
Prepublished online as a Blood First Edition Paper on May 30, 2006; DOI 10.1182/blood-2006-04-016444.


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Submitted April 11, 2006
Accepted May 9, 2006

Kinin receptor expression during Staphylococcus aureus infection

Sara H. Bengtson, Stephen B Phagoo, Anna Norrby-Teglund, Lisa Pahlman, Matthias Morgelin, Bruce L. Zuraw, Fredrik L. M. Leeb-Lundberg, and Heiko Herwald*

Lund University, Lund, Sweden
Angeles Research Institute, Los Angeles, USA
Karolinska Institute, Stockholm, Sweden
University of California, San Diego, USA

* Corresponding author; email: heiko.herwald{at}med.lu.se.

An 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 desArg9bradykinin. 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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J. Enquist, C. Skroder, J. L. Whistler, and L.M. F. Leeb-Lundberg
Kinins Promote B2 Receptor Endocytosis and Delay Constitutive B1 Receptor Endocytosis
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