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Infect Immun, February 1998, p. 866-869, Vol. 66, No. 2
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Involvement of Bradykinin Generation in Intravascular Dissemination of Vibrio vulnificus and Prevention of Invasion by a Bradykinin Antagonist

Keishi Maruo,1 Takaaki Akaike,2 Tomomichi Ono,1 and Hiroshi Maeda2,*

Departments of Microbiology2 and Dermatology,1 Kumamoto University School of Medicine, Kumamoto 860, Japan

Received 17 July 1997/Returned for modification 15 September 1997/Accepted 4 November 1997

Involvement of bradykinin generation in bacterial invasion was examined by using a gram-negative bacillus, Vibrio vulnificus, which is known to invade the blood circulatory system and cause septicemia. V. vulnificus was injected intraperitoneally (i.p.) into mice with or without bradykinin or a bradykinin (B2 receptor) antagonist. Dissemination of V. vulnificus from peritoneal septic foci to the circulating blood was assessed by counting of viable bacteria in venous blood by use of the colony-forming assay. Intravascular dissemination of V. vulnificus in mice was significantly potentiated by simultaneous injection with bradykinin but was markedly reduced by coadministration with the B2 antagonist D-Arg,[Hyp3, Thi5,8, D-Phe7]-bradykinin. Furthermore, V. vulnificus lethality was significantly increased when bradykinin was administered simultaneously with the bacillus, whereas it was definitely suppressed by treatment with D-Arg,[Hyp3, Thi5,8, D-Phe7]-bradykinin. Similarly, ovomacroglobulin, a potent inhibitor of the V. vulnificus protease, showed a strong suppressive effect on the V. vulnificus septicemia. We also confirmed appreciable bradykinin production in the primary septic foci in the mouse peritoneal cavity after i.p. inoculation with V. vulnificus. It is thus concluded that bradykinin generation in infectious foci is critically involved in facilitation of intravascular dissemination of V. vulnificus.

* Corresponding author. Mailing address: Department of Microbiology, Kumamoto University School of Medicine, Kumamoto 860, Japan. Phone: 81-96-373-5098. Fax: 81-96-362-8362. E-mail: msmaedah{at}gpo.kumamoto-u.ac.jp.




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