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

G. Haskó, L. Virág, G. Egnaczyk, A. L. Salzman, C. Szabó

Research output: Contribution to journalArticle

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 microg) 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-alpha, IL-1beta, IL-2, IL-6, IL-12 and IFN-gamma were significantly higher in the IL-10 KO mice than in the WT animals. The release of macrophage inflammatory proteins-1alpha 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)1417-1425
Number of pages9
JournalEuropean Journal of Immunology
Volume28
Issue number4
StatePublished - Apr 1998
Externally publishedYes

Fingerprint

Interleukin-10
Wild Animals
staphylococcal enterotoxin B
Shock
Anti-Inflammatory Agents
Chemokine CXCL2
Superantigens
Thymocytes
Interleukin-12
Interleukin-2
Immune System
Interleukin-6
Nitric Oxide
Cell Death
Tumor Necrosis Factor-alpha
Apoptosis
Cytokines

ASJC Scopus subject areas

  • Immunology

Cite this

The crucial role of IL-10 in the suppression of the immunological response in mice exposed to staphylococcal enterotoxin B. / Haskó, G.; Virág, L.; Egnaczyk, G.; Salzman, A. L.; Szabó, C.

In: European Journal of Immunology, Vol. 28, No. 4, 04.1998, p. 1417-1425.

Research output: Contribution to journalArticle

@article{8c7e81c128a44078baa79c58bbb68aed,
title = "The crucial role of IL-10 in the suppression of the immunological response in mice exposed to staphylococcal enterotoxin B.",
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 microg) 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-alpha, IL-1beta, IL-2, IL-6, IL-12 and IFN-gamma were significantly higher in the IL-10 KO mice than in the WT animals. The release of macrophage inflammatory proteins-1alpha 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.",
author = "G. Hask{\'o} and L. Vir{\'a}g and G. Egnaczyk and Salzman, {A. L.} and C. Szab{\'o}",
year = "1998",
month = "4",
language = "English (US)",
volume = "28",
pages = "1417--1425",
journal = "European Journal of Immunology",
issn = "0014-2980",
publisher = "Wiley-VCH Verlag",
number = "4",

}

TY - JOUR

T1 - The crucial role of IL-10 in the suppression of the immunological response in mice exposed to staphylococcal enterotoxin B.

AU - Haskó, G.

AU - Virág, L.

AU - Egnaczyk, G.

AU - Salzman, A. L.

AU - Szabó, C.

PY - 1998/4

Y1 - 1998/4

N2 - 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 microg) 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-alpha, IL-1beta, IL-2, IL-6, IL-12 and IFN-gamma were significantly higher in the IL-10 KO mice than in the WT animals. The release of macrophage inflammatory proteins-1alpha 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.

AB - 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 microg) 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-alpha, IL-1beta, IL-2, IL-6, IL-12 and IFN-gamma were significantly higher in the IL-10 KO mice than in the WT animals. The release of macrophage inflammatory proteins-1alpha 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.

UR - http://www.scopus.com/inward/record.url?scp=0032042306&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032042306&partnerID=8YFLogxK

M3 - Article

VL - 28

SP - 1417

EP - 1425

JO - European Journal of Immunology

JF - European Journal of Immunology

SN - 0014-2980

IS - 4

ER -