Interleukin-1 promotes hyperglycemia and insulitis in mice normally resistant to streptozotocin-induced diabetes

Susan J. Zunino, Linda F. Simons, Joseph F. Sambrook, Mary Jane H Gething

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

By administering physiological doses of interleukin-1 (IL-1) concurrently with multiple low doses of the β cell toxin streptozotocin (MSZ), we observed an augmentation of diabetes by IL-1 in four different strains of mice. Augmentation of hyperglycemia by IL-1 was most prominent in the two MSZ-resistant mouse strains Balb/cJ and A/J. Furthermore, concurrent treatment with IL-1 and MSZ rendered these MSZ-resistant mice susceptible to the development of significant insulitis when compared to mice treated with MSZ alone. Development of insulitis was dependent upon the dose of IL-1; it was only observed at an IL-1 dose of 250 ng/kg body weight. Analysis of the leukocytic infiltrate in the islets of mice after treatment with 250 ng/kg IL-1 plus MSZ revealed the presence of L3T4+ and Lyt-2+ T lymphocytes. Administration of MSZ alone or IL-1 alone did not produce diabetes in the MSZ-resistant mice, indicating that neither of these agents was toxic to the β cells by itself. We conclude that IL-1 synergizes with MSZ to augment diabetes in mice that are normally resistant to the diabetogenic effects of MSZ.

Original languageEnglish (US)
Pages (from-to)661-670
Number of pages10
JournalAmerican Journal of Pathology
Volume145
Issue number3
StatePublished - Sep 1994
Externally publishedYes

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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    Zunino, S. J., Simons, L. F., Sambrook, J. F., & Gething, M. J. H. (1994). Interleukin-1 promotes hyperglycemia and insulitis in mice normally resistant to streptozotocin-induced diabetes. American Journal of Pathology, 145(3), 661-670.