Staphylococcal enterotoxin B (SEB), a bacterial superantigen, activates the immune system resulting in a burst of pro- and anti-inflammatory cytokines. Using IL-10 deficient C57BL/6 (IL-10 KO) mice, we studied the role of endogenous IL-10 in the regulation of immune response to SEB. SEB (100 μg) induced the release of IL-10 in control C57BL/6 (IL-10 WT) mice, but not in the KO counterparts. SEB-evoked plasma levels of tumor necrosis factor-α, IL-1β, IL-2, IL-6, IL-12, and interferon-γ were significantly higher in the IL-10 KO mice than in WT animals. The release of macrophage inflammatory proteins -1α, and -2 were 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. Thus, IL-10 plays an important immunoregulatory role in response to a superantigenic stimulus, by dampening of the shock-inducing inflammatory response and early activation-induced cell death elicited by SEB.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Molecular Biology