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Infection and Immunity, September 2007, p. 4592-4596, Vol. 75, No. 9
0019-9567/07/$08.00+0 doi:10.1128/IAI.00481-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Department of Microbiology, Osaka University of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki, Osaka 569-1094, Japan,1 Department of Molecular Biopharmaceutical Sciences, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, 1-1-1 Tsushima-naka, Okayama 700-8530, Japan,2 Faculty of Pharmaceutical Sciences, Matsuyama University, 4-2 Bunkyo-cho, Matsuyama, Ehime 790-8578, Japan3
Received 3 April 2007/ Returned for modification 13 May 2007/ Accepted 17 June 2007
Vibrio vulnificus is an estuarine bacterium that can cause primary septicemia as well as serious wound infections. Generally, clinical isolates have a high lethal effect compared with environmental isolates. However, little is known about the mechanisms by which V. vulnificus causes disease. In this study, we compared the pathogenicity of a clinical isolate, strain M2799, with that of an environmental isolate, strain JCM3731. The clinical isolate showed 100 times higher lethality in mice than the environmental isolate. In strain M2799-inoculated mice, the number of macrophages decreased significantly, whereas there was no appreciable change in the number of macrophages in strain JCM3731-inoculated mice. The clinical isolate showed high cytotoxic activity, especially to macrophages, compared with the environmental isolate in vitro. The growth of the clinical isolate was almost completely inhibited in the presence of macrophages. Moreover, the survival rate of the clinical isolate-inoculated mice increased by recruitment of macrophages. These results indicate that V. vulnificus infection progresses by damage to macrophages during the early phase of infection.
Published ahead of print on 25 June 2007.
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