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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. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-04-016444v1 108/6/2055    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Bengtson, S. H. Articles by Herwald, H. Search for Related Content PubMed PubMed Citation Articles by Bengtson, S. H. Articles by Herwald, H. Related Collections Hemostasis, Thrombosis, and Vascular Biology Phagocytes Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PHAGOCYTES Kinin receptor expression during Staphylococcus aureus infection Sara H. Bengtson, Stephen B. Phagoo, Anna Norrby-Teglund, Lisa Påhlman, Matthias Mörgelin, Bruce L. Zuraw, L. M. Fredrik Leeb-Lundberg, and Heiko Herwald From the Department of Clinical Sciences, Section for Clinical and Experimental Infection Medicine, and the Department of Experimental Medical Science, Division of Cellular and Molecular Pharmacology, Lund University, Sweden; the Developmental Biology Program, Childrens Hospital Los Angeles Research Institute, Los Angeles, CA; Karolinska Institutet, Center for Infectious Medicine, Huddinge University Hospital, Stockholm, Sweden; and the Department of Medicine, Veterans Affairs Medical Center and University of California, San Diego, CA. 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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Sanden, J. Enquist, S. H. Bengtson, H. Herwald, and L. M. F. Leeb-Lundberg Kinin B2 Receptor-Mediated Bradykinin Internalization and Metalloendopeptidase EP24.15-Dependent Intracellular Bradykinin Degradation J. Pharmacol. Exp. Ther., July 1, 2008; 326(1): 24 - 32. [Abstract] [Full Text] [PDF] J. Enquist, C. Skroder, J. L. Whistler, and L.M. F. Leeb-Lundberg Kinins Promote B2 Receptor Endocytosis and Delay Constitutive B1 Receptor Endocytosis Mol. Pharmacol., February 1, 2007; 71(2): 494 - 507. [Abstract] [Full Text] [PDF]

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