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European Journal of Heart Failure Advance Access originally published online on January 16, 2009
European Journal of Heart Failure 2009 11(3):229-237; doi:10.1093/eurjhf/hfn049
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Suppression of inflammation in rat autoimmune myocarditis by S100A8/A9 through modulation of the proinflammatory cytokine network

Kaoru Otsuka1, Fumio Terasaki1,*, Masaki Ikemoto2, Shuichi Fujita1, Bin Tsukada1, Takashi Katashima1, Yumiko Kanzaki1, Koichi Sohmiya1, Tatsuji Kono1, Haruhiro Toko3, Masatoshi Fujita2 and Yasushi Kitaura1

1 Department of Internal Medicine III, Osaka Medical College, 2-7 Daigaku-machi, Takatsuki 569-8686, Japan
2 Human Health Sciences, Kyoto University Graduate School of Medicine, Japan
3 Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, Japan

* Corresponding author. Tel: +81 72 683 1221, Fax: +81 72 684 6598, Email: in3012{at}poh.osaka-med.ac.jp


  Abstract

Aims: S100A8/A9 is expressed in activated monocytes/macrophages and assumed to be heavily involved in the pathogenesis of acute inflammation. Although several studies have asserted that S100A8/A9 has a proinflammatory function, the exact biological function of S100A8/A9 is yet to be described. We examined the anti-inflammatory effects of S100A8/A9 on experimental autoimmune myocarditis (EAM) in rats.

Methods and results: Experimental autoimmune myocarditis was induced in Lewis rats by immunization with porcine cardiac myosin. The recombinant (R-) S100A8/A9 was injected intraperitoneally into EAM rats. R-S100A8/A9 attenuated the severity of myocarditis, as evidenced by echocardiographic and histological findings. In addition, we found that not only the mRNA expression of proinflammatory cytokines [interleukin (IL)-1β, IL-6, and tumour necrosis factor (TNF)-{alpha}] in the myocardium, but also their serum concentrations were suppressed in EAM rats treated with R-S100A8/A9. Nuclear factor-kappa B expression in inflammatory cells was also suppressed in the treated rats. To elucidate the mechanistic function of S100A8/A9 on proinflammatory cytokines in vivo, we used an ELISA on the supernatant of homogenized heart tissue treated with R-S100A8/A9. The findings revealed high-affinity binding of R-S100A8/A9 with IL-1β, IL-6, and TNF-{alpha} in the myocardium, suggesting the trapping of proinflammatory cytokines by R-S100A8/A9.

Conclusion: S100A8/A9 attenuates EAM through modulation of the proinflammatory cytokine network.

Key Words: S100A8/A9 • Autoimmune myocarditis • Cytokines • Inflammation

Received July 31, 2008; Revised September 11, 2008; Accepted November 20, 2008


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