The crucial role of IL-10 in the suppression of the immunological response in mice exposed to staphylococcal enterotoxin B

György Haskó, László Virág, Gregory Egnaczyk, Andrew L. Salzman, Csaba Szabo

Research output: Contribution to journalArticle

62 Scopus citations

Abstract

Staphylococcal enterotoxin B (SEB), a bacterial superantigen, activates the immune system resulting in a burst of pro- and anti-inflammatory cytokines. A central anti-inflammatory mediator in this process is IL-10. Using IL-10-deficient C57BL/6 (IL-10 KO) mice, we studied the role of endogenous IL-10 in the regulation of the immune response to SEB. SEB (100 μg) induced the release of IL-10 in control C57BL/6 [IL-10 wild type (WT)] mice, but not in their IL-10 KO counterparts. SEB-evoked plasma levels of TNF-α, IL-1β, IL-2, IL-6, IL-12 and IFN-γ were significantly higher in the IL-10 KO mice than in the WT animals. The release of mac rophage inflammatory proteins-1α and -2 was also enhanced in the IL-10 KO mice. Further, upon SEB challenge, mice deficient in IL-10 produced higher levels of nitric oxide than the WT animals. IL-10 deficiency resulted in a marked enhancement of the SEB-induced apoptosis of thymocytes. Finally, IL-10 KO mice were more susceptible to SEB-induced lethal shock than their WT controls. These results show that IL-10 plays an important immunoregulatory role in the response to a superantigenic stimulus, by dampening of the shock-inducing inflammatory response and early activation-induced cell death elicited by SEB.

Original languageEnglish (US)
Pages (from-to)1415-1423
Number of pages9
JournalEuropean Journal of Immunology
Volume28
Issue number4
StatePublished - Apr 1998
Externally publishedYes

Keywords

  • Cytokine
  • IL-10
  • IL-12
  • Inflammation
  • Macrophage inflammatory protein

ASJC Scopus subject areas

  • Immunology

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