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Infection and Immunity, May 2003, p. 2542-2547, Vol. 71, No. 5
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.5.2542-2547.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Staphylococcal Enterotoxin B-Induced Acute Inflammation Is Inhibited by Dexamethasone: Important Role of CXC Chemokines KC and Macrophage Inflammatory Protein 2

Rene Schramm and Henrik Thorlacius*

Department of Surgery, Malmö University Hospital, Lund University, Malmö, Sweden

Received 23 September 2002/ Returned for modification 3 December 2002/ Accepted 7 January 2003

This study was conducted to examine the anti-inflammatory mechanisms of dexamethasone during leukocyte recruitment and expression of the CXC chemokines macrophage inflammatory protein 2 (MIP-2) (CXCL2) and cytokine-induced neutrophil chemoattractant (KC) (CXCL1) in staphylococcal enterotoxin B (SEB)-induced acute inflammation. To do this, SEB was injected into murine air pouches with or without dexamethasone pretreatment for 2 h. SEB induced infiltration of leukocytes in a dose- and time-dependent manner, with the maximal response observed after 4 h of treatment with 10 µg of SEB. The recruited leukocytes comprised more than 77% neutrophils. Moreover, SEB challenge (10 µg) provoked time-dependent secretion of CXC chemokines, which peaked after 1 h. Local administration of antibodies against MIP-2 and KC significantly reduced SEB-triggered neutrophil accumulation by 38 and 59%, respectively. Dexamethasone (10 mg kg-1) significantly decreased neutrophil recruitment by 82% and reduced secretion of MIP-2 and KC by 89 and 85%, respectively, in response to SEB challenge. Our data demonstrate that dexamethasone potently inhibits neutrophil recruitment in SEB-induced inflammation. Moreover, we provide evidence that MIP-2 and KC are key mediators in the neutrophil response to SEB. Furthermore, our findings demonstrate that dexamethasone attenuates SEB-induced expression of MIP-2 and KC. Thus, this study elucidates important signaling pathways of SEB-induced neutrophil recruitment and anti-inflammatory mechanisms of action of dexamethasone.

* Corresponding author. Mailing address: Department of Surgery, Malmö University Hospital, SE-20502 Malmö, Sweden. Phone: 46-40-332077. Fax: 46-40-336207. E-mail: henrikthorlacius{at}hotmail.com.

Editor: A. D. O'Brien

Infection and Immunity, May 2003, p. 2542-2547, Vol. 71, No. 5
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.5.2542-2547.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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