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Infection and Immunity, January 2009, p. 327-334, Vol. 77, No. 1
0019-9567/09/$08.00+0 doi:10.1128/IAI.00748-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Department of Bacteriology, Jikei University School of Medicine, Minato-ku, Tokyo 105-8461, Japan
Received 16 June 2008/ Returned for modification 18 July 2008/ Accepted 10 October 2008
Neutrophils play a crucial role in the host response to infection with Staphylococcus aureus, which is a major human pathogen capable of causing life-threatening disease. Interleukin-8 (IL-8) is a potent chemoattractant and activator of neutrophils. We previously reported that S. aureus secretes a factor that suppresses IL-8 production by human endothelial cells. Here we isolated an inhibitor of IL-8 production from the supernatant and identified it as staphylococcal beta-hemolysin. Beta-hemolysin reduced IL-8 production without cytotoxicity to endothelial cells. Pretreatment with beta-hemolysin decreased the expression of both IL-8 mRNA and protein induced by tumor necrosis factor alpha (TNF-
). Migration of neutrophils across TNF-
-activated endothelium was also inhibited by beta-hemolysin. In contrast, beta-hemolysin had no effect on intercellular adhesive molecule 1 expression in activated endothelial cells. These results showed that beta-hemolysin produced by S. aureus interferes with inflammatory signaling in endothelial cells and may help S. aureus evade the host immune response.
Published ahead of print on 20 October 2008.
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