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Clinical and Diagnostic Laboratory Immunology, November 2002, p. 1307-1312, Vol. 9, No. 6
1071-412X/02/$04.00+0     DOI: 10.1128/CDLI.9.6.1307-1312.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Primary Role of Interleukin-1 and Interleukin-1ß in Lipopolysaccharide-Induced Hypoglycemia in Mice

Senri Oguri,^1,2 Katsutoshi Motegi,² Yoichiro Iwakura,³ and Yasuo Endo^1*

Departments of Pharmacology,¹ Maxillofacial and Plastic Surgery, Graduate School of Dentistry, Tohoku University, 4-1 Seiryo-Machi, Aoba-Ku, Sendai 980-8575,² Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Minato-Ku, Tokyo 108-8639, Japan³

Received 9 October 2001/ Returned for modification 23 April 2002/ Accepted 5 July 2002

Within a few hours of its injection into mice, lipopolysaccharide (LPS) induces hypoglycemia and the production of various cytokines. We previously found that interleukin-1 (IL-1), IL-1ß, and tumor necrosis factor alpha (TNF-) induce hypoglycemia and that the minimum effective dose of IL-1 or IL-1ß is about 1/1,000 that of TNF-. In the present study, we examined the contribution made by IL-1 to the hypoglycemic action of LPS. Nine other cytokines tested were all inactive at inducing hypoglycemia. LPS produced hypoglycemia in mice deficient in either IL-1 or IL-1ß but not in mice deficient in both cytokines (IL-1 and -1ß knockout [IL-1/ß KO] mice). IL-1, IL-1ß, and TNF- induced hypoglycemia in IL-1/ß KO mice, as they did in normal control mice. The LPS-induced elevation of serum cortisol was weaker in IL-1/ß KO mice than in control mice, and, in the latter, serum cortisol was markedly raised while blood glucose was declining. IL-1 decreased blood glucose both in NOD mice (which have impaired insulin production) and in KK-Ay mice (insulin resistant). These results suggest that (i) cortisol may not be involved in mediating the resistance of IL-1/ß KO mice to the hypoglycemic action of LPS, (ii) as a mediator, IL-1 is a prerequisite for the hypoglycemic action of LPS, (iii) IL-1 and IL-1ß perform mutual compensation, and (iv) IL-1 plays a role as the primary stimulator of the many anabolic reactions required for the elaboration of immune responses against infection.

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* Corresponding author. Mailing address: Department of Pharmacology, Graduate School of Dentistry, Tohoku University, 4-1 Seiryo-Machi, Aoba-Ku, Sendai 980, Japan. Fax: 81-22-717-8313. E-mail: endo{at}pharmac.dent.tohoku.ac.jp.

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Clinical and Diagnostic Laboratory Immunology, November 2002, p. 1307-1312, Vol. 9, No. 6
1071-412X/02/$04.00+0     DOI: 10.1128/CDLI.9.6.1307-1312.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

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