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Infection and Immunity, May 2000, p. 2424-2430, Vol. 68, No. 5
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Interleukin-4 and Interleukin-10 Are Involved in Host Resistance to Staphylococcus aureus Infection through Regulation of Gamma Interferon

Sanae Sasaki,1 Shinsuke Nishikawa,1,dagger Tomisato Miura,1,2 Mayuko Mizuki,1 Kyogo Yamada,1 Hiroo Madarame,3 Yoh-Ichi Tagawa,4 Yoichiro Iwakura,5 and Akio Nakane1,*

Department of Bacteriology, Hirosaki University School of Medicine,1 and School of Allied Medical Sciences Hirosaki University,2 Hirosaki, Veterinary Teaching Hospital, Azabu University, Sagamihara,3 Institute of Experimental Animals, Shinshu University School of Medicine, Matsumoto,4 and Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo,5 Japan

Received 8 October 1999/Returned for modification 6 December 1999/Accepted 25 January 2000

Our previous study showed that gamma interferon (IFN-gamma ), a T-helper 1 (Th1)-type cytokine, plays a detrimental role in Staphylococcus aureus infection in mice. In this study, the role of Th2-type cytokines such as interleukin-4 (IL-4) and IL-10 in S. aureus infection was investigated. IL-10 mRNA was induced in parallel with IFN-gamma in the spleens and kidneys of mice during S. aureus infection, whereas IL-4 mRNA was induced in the spleens but not in the kidneys of these animals. Spleen cells obtained from S. aureus-infected mice produced lower titers of IFN-gamma and higher titers of IL-4 and IL-10 in response to heat-killed S. aureus than did those from uninfected mice. Administration of anti-IL-4 monoclonal antibody (MAb) or anti-IL-10 MAb inhibited the elimination of S. aureus cells from the kidneys of mice. IFN-gamma mRNA expression was enhanced in the spleens of anti-IL-4 MAb- or anti-IL-10 MAb-treated mice and also in the kidneys of anti-IL-4 MAb-treated animals. Next, we evaluated the role of IFN-gamma in S. aureus infection in IFN-gamma -/- mice. An increase in survival rates, a decrease in bacterial numbers in the kidneys, and an amelioration of histologic abnormalities in these organs were observed in IFN-gamma -/- mice compared with those in IFN-gamma +/+ mice. Administration of MAb against IL-4 or IL-10 failed to affect bacterial growth in the spleens and kidneys of IFN-gamma -/- mice irrespective of the expression of Th2 response. These results suggest that S. aureus infection induced a Th2 response and that IL-4 and IL-10 might play a protective role through the regulation of IFN-gamma in S. aureus infection.

* Corresponding author. Mailing address: Department of Bacteriology, Hirosaki University School of Medicine, Zaifu-cho 5, Hirosaki, Aomori 036-8562, Japan. Phone: 81-172-39-5032. Fax: 81-172-39-5034. e-mail: a27k03n0{at}cc.hirosaki-u.ac.jp.

dagger Present address: Second Department of Surgery, Hirosaki University School of Medicine, Hirosaki, Japan.

Infection and Immunity, May 2000, p. 2424-2430, Vol. 68, No. 5
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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