This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Hirata, N. Articles by Nasu, M. Search for Related Content PubMed PubMed Citation Articles by Hirata, N. Articles by Nasu, M.

 Previous Article  |  Next Article 

Antimicrobial Agents and Chemotherapy, September 2001, p. 2638-2642, Vol. 45, No. 9
0066-4804/01/$04.00+0   DOI: 10.1128/AAC.45.9.2638-2642.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Pretreatment of Mice with Clindamycin Improves Survival of Endotoxic Shock by Modulating the Release of Inflammatory Cytokines

Norio Hirata, Kazufumi Hiramatsu, Kenji Kishi, Tohru Yamasaki, Tomoku Ichimiya, and Masaru Nasu^*

Second Department of Internal Medicine, Oita Medical University, Hasama, Oita 879-5593, Japan

Received 27 December 2000/Returned for modification 2 March 2001/Accepted 31 May 2001

Suppression of endotoxin release and subsequent production of inflammatory cytokines is crucial in the treatment of septic shock. We investigated the effect of clindamycin (CLI) on endotoxic shock induced in mice by Escherichia coli lipopolysaccharide (LPS). Mice were treated with CLI (160 to 600 mg/kg) or saline and then injected with E. coli LPS and D-(+)-galactosamine intraperitoneally 0.5 h after CLI administration. Pretreatment with CLI significantly improved survival in a dose-dependent manner (CLI, at 160, 300, and 440 mg/kg) and significantly lowered the peak concentrations of tumor necrosis factor alpha and interleukin-1 (IL-1) in serum. However, the peak concentrations of IL-6 in the sera of CLI-treated mice were higher than in control mice. Our findings suggest that CLI alters LPS-induced inflammatory cytokine production and suppresses endotoxin-induced mortality in this murine model.

---

^* Corresponding author. Mailing address: Second Department of Internal Medicine, Oita Medical University, Hasama, Oita 879-5593, Japan. Phone: 81-97-586-5804. Fax: 81-97-549-4245. E-mail: mnasu{at}oita-med.ac.jp.

---

Antimicrobial Agents and Chemotherapy, September 2001, p. 2638-2642, Vol. 45, No. 9
0066-4804/01/$04.00+0   DOI: 10.1128/AAC.45.9.2638-2642.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

This article has been cited by other articles:

• Burnett, A. M., Domachowske, J. B. (2007). Therapeutic Considerations for Children With Invasive Group A Streptococcal Infections: A Case Series Report and Review of the Literature. CLIN PEDIATR 46: 550-555  
• Brook, I., Germana, A., Giraldo, D. E., Camp-Hyde, T. D., Bolduc, D. L., Foriska, M. A., Elliott, T. B., Thakar, J. H., Shoemaker, M. O., Jackson, W. E., Ledney, G. D. (2005). Clindamycin and quinolone therapy for Bacillus anthracis Sterne infection in 60Co-gamma-photon-irradiated and sham-irradiated mice. J Antimicrob Chemother 56: 1074-1080 [Abstract] [Full Text]  
• Silverstein, R. (2004). Review: D-Galactosamine lethality model: scope and limitations. Innate Immunity 10: 147-162 [Abstract]  
• Nakano, T., Hiramatsu, K., Kishi, K., Hirata, N., Kadota, J.-i., Nasu, M. (2003). Clindamycin Modulates Inflammatory-Cytokine Induction in Lipopolysaccharide-Stimulated Mouse Peritoneal Macrophages. Antimicrob. Agents Chemother. 47: 363-367 [Abstract] [Full Text]  
• Araujo, F. G., Slifer, T. L., Remington, J. S. (2002). Inhibition of Secretion of Interleukin-1{alpha} and Tumor Necrosis Factor Alpha by the Ketolide Antibiotic Telithromycin. Antimicrob. Agents Chemother. 46: 3327-3330 [Abstract] [Full Text]