This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Mehindate, K Articles by Mourad, W Search for Related Content PubMed PubMed Citation Articles by Mehindate, K Articles by Mourad, W

 Previous Article  |  Next Article 

Infection and Immunity, November 1994, p. 4716-4721, Vol. 62, No. 11
0019-9567/1994/$04.00+0     DOI:

research-article

Modulation of Mycoplasma arthritidis-derived superantigen-induced cytokine gene expression by dexamethasone and interleukin-4.

Département de Médecine, Université Laval, St-Foy, Québec, Canada.

ABSTRACT

Activation of human monocytes or monocytic cell lines with all known stimuli coordinately induces the gene expression of various cytokines, including tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and the IL-1 receptor antagonist (IL-1Ra). In contrast, superantigens induce TNF-alpha and IL-1 beta but fail to affect IL-1Ra gene expression, suggesting that activation of monocytes via major histocompatibility complex class II is distinct from other signal transduction pathways. In the present study, we analyzed the regulation of the Mycoplasma arthritidis-derived superantigen (MAM)-induced IL-1 beta and TNF-alpha gene expression by studying the effects of two different anti-inflammatory agents: dexamethasone (DEX) and the T-cell-derived cytokine IL-4. Both agents contributed to the downregulation of MAM-induced IL-1 beta and TNF-alpha gene expression. They accelerated the normal decline of the gene expression of both MAM-induced cytokines by decreasing the stability of mRNAs via the induction or enhanced synthesis of one or more regulatory proteins. In addition, IL-4, but not DEX, induced a strong and rapid expression of IL-1Ra mRNA in MAM-stimulated and unstimulated THP-1 cells in a de novo protein synthesis-independent manner. The capacity of IL-4 to induce IL-1Ra gene expression reinforces its anti-inflammatory activity. This study illustrates some of the mechanisms by which MAM-induced proinflammatory monokine gene expression can be downregulated by IL-4 and DEX.

This article has been cited by other articles:

• Bouillon, M., El Fakhry, Y., Girouard, J., Khalil, H., Thibodeau, J., Mourad, W. (2003). Lipid Raft-dependent and -independent Signaling through HLA-DR Molecules. J. Biol. Chem. 278: 7099-7107 [Abstract] [Full Text]  
• Mu, H.-H., Sawitzke, A. D., Cole, B. C. (2001). Presence of Lpsd Mutation Influences Cytokine Regulation In Vivo by the Mycoplasma arthritidis Mitogen Superantigen and Lethal Toxicity in Mice Infected with M. arthritidis. Infect. Immun. 69: 3837-3844 [Abstract] [Full Text]  
• Razin, S., Yogev, D., Naot, Y. (1998). Molecular Biology and Pathogenicity of Mycoplasmas. Microbiol. Mol. Biol. Rev. 62: 1094-1156 [Abstract] [Full Text]