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International Immunology Advance Access published online on March 28, 2006
International Immunology, doi:10.1093/intimm/dxl004
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© The Japanese Society for Immunology. 2006. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org
Received October 3, 2005
Accepted January 31, 2006

Article

c-Fos suppresses systemic inflammatory response to endotoxin

Neelanjan Ray 1, Masayoshi Kuwahara 2, Yasunari Takada 3, Kenta Maruyama 3, Tomohiro Kawaguchi 2, Hirokazu Tsubone 2, Hiromichi Ishikawa 3, and Koichi Matsuo 3 *

1 Department of Microbiology and Immunology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, 160-8582 Tokyo, Japan; Medical Scholars Program, Vanderbilt University School of Medicine, Nashville, TN 37232-8300, USA
2 Department of Comparative Pathophysiology, Graduate School of Agricultural and Life Sciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, 113-8657 Tokyo, Japan
3 Department of Microbiology and Immunology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, 160-8582 Tokyo, Japan

* To whom correspondence should be addressed.
Koichi Matsuo, E-mail: matsuo{at}sc.itc.keio.ac.jp


  Abstract

We explored the role of the transcription factor c-Fos in lipopolysaccharide (LPS)-induced cytokine response using mice lacking c-Fos (Fos-/- mice). Compared with wild-type controls, Fos-/- macrophages and mice showed significantly enhanced production of tumour necrosis factor (TNF)-{alpha}, interleukin (IL)-6 and IL-12 p40, but reduced production of the anti-inflammatory cytokine IL-10. Bandshift analysis revealed that LPS-induced NF-{kappa}B binding activity to a functional site in the TNF-{alpha} promoter was significantly higher in Fos-/- than in wild-type macrophages. Using telemetry, we monitored body temperature and heart rate after LPS injection and found that Fos-/- mice undergo more severe hypothermia and bradycardia than wild-type mice. Such shock responses in Fos-/- mice were significantly reversed by neutralizing TNF-{alpha}. These data reveal a novel in vivo role for c-Fos as an anti-inflammatory transcription factor acting through suppression of NF-{kappa}B activity.

Keywords: AP-1; body temperature; cytokines; knockout mice; NF-{kappa}B; telemetry; TNF-{alpha}.
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