Staphylococcal enterotoxin B and tumor-necrosis factor-alpha-induced relapses of experimental allergic encephalomyelitis: protection by transforming growth factor-beta and interleukin-10 - PubMed (original) (raw)

. 1995 Nov;25(11):3035-40.

doi: 10.1002/eji.1830251108.

Affiliations

• PMID: 7489740
• DOI: 10.1002/eji.1830251108

Staphylococcal enterotoxin B and tumor-necrosis factor-alpha-induced relapses of experimental allergic encephalomyelitis: protection by transforming growth factor-beta and interleukin-10

G M Crisi et al. Eur J Immunol. 1995 Nov.

Abstract

A study was made of the ability of the superantigen staphylococcal enterotoxin B (SEB) to induce relapses of experimental allergic encephalomyelitis (EAE) in SJL mice that had partially or completely recovered from acute EAE. We find that a single injection of 0.05 mg SEB i.v. induces mild relapses in 50% of such mice. In addition, tumor necrosis factor (TNF)-alpha (0.2 micrograms, i.p.) also induces EAE relapses in 43% of SJL mice when injected 1-2 months after recovery. SEB does not induce a second relapse if reinjected when V beta 17a+T cells are still partially deleted. In these mice, however, TNF-alpha is equally effective in inducing relapses as in mice that did not receive SEB previously. We showed earlier that transforming growth factor (TGF)-beta and TNF-alpha have antagonistic effects on experimental autoimmune diseases; e.g., in spontaneously relapsing EAE, TGF-beta and anti-TNF were protective, while anti-TGF-beta caused disease exacerbation. Interleukin (IL)-10 is also known to counteract certain TNF effects. We now find that both human IL-10 and TGF-beta 2 lower the incidence of EAE relapses when given simultaneously with SEB or TNF-alpha. The protective effect of TGF-beta is significant only against relapses induced by SEB (reduced to 9%), and that of IL-10 only against relapses induced by TNF (reduced to 0%) with the treatment regimens employed. Neutralizing anti-TGF-beta does not increase the incidence of SEB-induced EAE relapses. In contrast, anti-IL-10 increases both the incidence and the severity of such relapses. We conclude that TNF production is probably important in causing EAE relapses, but that other aspects of the SEB-induced reactivation of myelin-specific T cells also contribute. Furthermore, endogenous IL-10 rather than TGF-beta production appears to limit the susceptibility to induction of EAE relapses in this model.

PubMed Disclaimer

Similar articles

• Studies on the mechanisms by which transforming growth factor-beta (TGF-beta) protects against allergic encephalomyelitis. Antagonism between TGF-beta and tumor necrosis factor.
  Santambrogio L, Hochwald GM, Saxena B, Leu CH, Martz JE, Carlino JA, Ruddle NH, Palladino MA, Gold LI, Thorbecke GJ. Santambrogio L, et al. J Immunol. 1993 Jul 15;151(2):1116-27. J Immunol. 1993. PMID: 8335893
• Antibodies against IL-12 prevent superantigen-induced and spontaneous relapses of experimental autoimmune encephalomyelitis.
  Constantinescu CS, Wysocka M, Hilliard B, Ventura ES, Lavi E, Trinchieri G, Rostami A. Constantinescu CS, et al. J Immunol. 1998 Nov 1;161(9):5097-104. J Immunol. 1998. PMID: 9794448
• Induction of relapsing paralysis in experimental autoimmune encephalomyelitis by bacterial superantigen.
  Brocke S, Gaur A, Piercy C, Gautam A, Gijbels K, Fathman CG, Steinman L. Brocke S, et al. Nature. 1993 Oct 14;365(6447):642-4. doi: 10.1038/365642a0. Nature. 1993. PMID: 7692305
• Antagonistic effects of endogenous and exogenous TGF-beta and TNF on auto-immune diseases in mice.
  Santambrogio L, Hochwald GM, Leu CH, Thorbecke GJ. Santambrogio L, et al. Immunopharmacol Immunotoxicol. 1993 Aug;15(4):461-78. doi: 10.3109/08923979309035240. Immunopharmacol Immunotoxicol. 1993. PMID: 8227972
• Laboratory exposures to staphylococcal enterotoxin B.
  Rusnak JM, Kortepeter M, Ulrich R, Poli M, Boudreau E. Rusnak JM, et al. Emerg Infect Dis. 2004 Sep;10(9):1544-9. doi: 10.3201/eid1009.040250. Emerg Infect Dis. 2004. PMID: 15498154 Free PMC article. Review.

Cited by

• IL-5 induces proliferation and activation of microglia via an unknown receptor.
  Liva SM, de Vellis J. Liva SM, et al. Neurochem Res. 2001 Jun;26(6):629-37. doi: 10.1023/a:1010983119125. Neurochem Res. 2001. PMID: 11523538
• Role of cytokines as mediators and regulators of microglial activity in inflammatory demyelination of the CNS.
  Merson TD, Binder MD, Kilpatrick TJ. Merson TD, et al. Neuromolecular Med. 2010 Jun;12(2):99-132. doi: 10.1007/s12017-010-8112-z. Epub 2010 Mar 30. Neuromolecular Med. 2010. PMID: 20411441 Review.
• Role of pathogenic T cells and autoantibodies in relapse and progression of myelin oligodendrocyte glycoprotein-induced autoimmune encephalomyelitis in LEW.1AV1 rats.
  Matsumoto Y, Park IK, Hiraki K, Ohtani S, Kohyama K. Matsumoto Y, et al. Immunology. 2009 Sep;128(1 Suppl):e250-61. doi: 10.1111/j.1365-2567.2008.02955.x. Epub 2008 Oct 29. Immunology. 2009. PMID: 19175799 Free PMC article.
• Pathophysiology and Therapeutic Approaches for Spinal Cord Injury.
  Lima R, Monteiro A, Salgado AJ, Monteiro S, Silva NA. Lima R, et al. Int J Mol Sci. 2022 Nov 10;23(22):13833. doi: 10.3390/ijms232213833. Int J Mol Sci. 2022. PMID: 36430308 Free PMC article. Review.
• Interleukin-12 induces relapse in experimental allergic encephalomyelitis in the Lewis rat.
  Smith T, Hewson AK, Kingsley CI, Leonard JP, Cuzner ML. Smith T, et al. Am J Pathol. 1997 Jun;150(6):1909-17. Am J Pathol. 1997. PMID: 9176384 Free PMC article.

Publication types

MeSH terms

Substances

LinkOut - more resources

• Full Text Sources

  • Wiley

• Other Literature Sources

  • The Lens - Patent Citations Database

• Molecular Biology Databases

  • Mouse Genome Informatics (MGI)