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Antimicrobial Agents and Chemotherapy, November 1998, p. 2853-2857, Vol. 42, No. 11
0066-4804/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Effect of Interleukin-10 on Gut-Derived Sepsis Caused by Pseudomonas aeruginosa in Mice

Tetsuya Matsumoto,1,* Kazuhiro Tateda,1 Shuichi Miyazaki,1 Nobuhiko Furuya,1 Akira Ohno,1 Yoshikazu Ishii,1 Yoichi Hirakata,2 and Keizo Yamaguchi1

Department of Microbiology, Toho University School of Medicine, Omori-Nishi, Ota-ku, Tokyo,1 and Department of Laboratory Medicine, Nagasaki University School of Medicine, Sakamoto, Nagasaki,2 Japan

Received 22 April 1998/Returned for modification 4 June 1998/Accepted 2 September 1998

We evaluated the protective effect of interleukin-10 (IL-10) against murine gut-derived sepsis caused by Pseudomonas aeruginosa. Gut-derived sepsis was induced by administering cyclophosphamide and ampicillin while feeding P. aeruginosa to specific-pathogen-free mice. Treating mice with recombinant human IL-10 (rhIL-10) at 1.0 or 5.0 µg/mouse twice a day following the second cyclophosphamide administration significantly increased the survival rate compared to that of control mice treated with saline; however, treatment with rhIL-10 at 0.1 µg/mouse did not result in significant protection. Bacterial counts in the liver, spleen, and blood were all significantly lower in mice treated with rhIL-10 than in saline-treated control mice. Treatment with rhIL-10 significantly suppressed tumor necrosis factor alpha, interleukin-1beta , interleukin-6, and gamma interferon levels in the serum of mice following induction of gut-derived sepsis. We also studied the effect of IL-10 on leukocyte recovery after cyclophosphamide treatment of mice. Administration of rhIL-10 intraperitoneally at 1.0 µg/mouse significantly accelerated the recovery of leukocytes in comparison with that of the group of saline-treated controls. These results indicate that IL-10 shows a protective effect against gut-derived P. aeruginosa sepsis. We suspect that the mechanism of this effect is that IL-10 regulates in vivo production of inflammatory cytokines. Furthermore, acceleration of leukocyte recovery by IL-10 after cyclophosphamide-induced depression may also play an important role in this protection.

* Corresponding author. Mailing address: Department of Microbiology, Toho University School of Medicine, 5-21-16 Omori-Nishi, Ota-ku, Tokyo 143-8540, Japan. Phone: 81-3-3762-4151, ext. 2396. Fax: 81-3-5493-5415. E-mail: tetsu{at}med.toho-u.ac.jp.

Antimicrobial Agents and Chemotherapy, November 1998, p. 2853-2857, Vol. 42, No. 11
0066-4804/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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