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Infect Immun, March 1998, p. 1017-1022, Vol. 66, No. 3
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Protective Role of Nitric Oxide in Staphylococcus aureus Infection in Mice

Sanae Sasaki,¹ Tomisato Miura,^1,2 Shinsuke Nishikawa,¹ Kyogo Yamada,¹ Mayuko Hirasue,¹ and Akio Nakane^1,*

Department of Bacteriology, School of Medicine,¹ and School of Allied Medical Sciences,² Hirosaki University, Hirosaki 036, Japan

Received 28 July 1997/Returned for modification 3 September 1997/Accepted 22 December 1997

This study was carried out to determine the role of nitric oxide (NO) in Staphylococcus aureus infection in mice. NO production in spleen cell cultures was induced by heat-killed S. aureus. Expression of mRNA of the inducible isoform of NO synthase (iNOS) was induced in the spleens and kidneys of S. aureus-infected mice. When mice were treated with monoclonal antibodies (MAbs) against tumor necrosis factor alpha (TNF-) or gamma interferon (IFN-) before S. aureus infection, the induction of iNOS mRNA expression in the kidneys was inhibited. These MAbs also inhibited NO production in spleen cell cultures stimulated with heat-killed S. aureus. NO production in the spleen cell cultures and levels of urinary nitrate plus nitrite were suppressed by treatment with aminoguanidine (AG), a selective inhibitor of iNOS. The survival rates of AG-treated mice were significantly decreased by either lethal or sublethal S. aureus infections. However, an effect of AG administration on bacterial growth was not observed in the spleens and kidneys of mice during either type of infection. Production of TNF- and IFN- was not affected by AG treatment in vitro and in vivo. These results suggest that NO plays an important role in protection from lethality by the infection, but the protective role of NO in host resistance against S. aureus infection was not proved. Moreover, our results show that TNF- and IFN- regulate NO production while NO may not be involved in the regulation of the production of these cytokines during S. aureus infection.

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^* Corresponding author. Mailing address: Department of Bacteriology, Hirosaki University School of Medicine, Zaifu-cho 5, Hirosaki 036, Japan. Phone: 81-172-39-5032. Fax: 81-172-39-5034. E-mail: a27k03n0{at}cc.hirosaki-u.ac.jp.

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