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 Bras, A. Articles by Martinez-A, C. Search for Related Content PubMed PubMed Citation Articles by Bras, A. Articles by Martinez-A, C.

 Previous Article  |  Next Article 

Infect. Immun., 10 1997, 4030-4037, Vol 65, No. 10
Copyright © 1997, American Society for Microbiology

Nitric oxide regulates clonal expansion and activation-induced cell death triggered by staphylococcal enterotoxin B

A Bras, L Rodriguez-Borlado, A Gonzalez-Garcia and C Martinez-A
Department of Immunology and Oncology, National Center for Biotechnology, CSIC, Universidad Autonoma, Cantoblanco Campus, Madrid, Spain. abras@cnb.uam.es

Increased interest has recently been focused on nitric oxide (NO) due to its several biological roles. Apart from being a potential antimicrobial defense and a mediator of autoimmune diseases, NO also appears to be a strong mediator of T-cell responses. In this report, we have characterized the effect of NO on T-cell function. For this purpose, we analyzed in vivo T-cell responses to the bacterial superantigen produced by Staphylococcus aureus, staphylococcal enterotoxin B (SEB), in mice treated with an NO donor (isosorbide dinitrate [ISO]). We show that ISO partially prevents SEB-triggered activation-induced cell death of spleen and lymph node CD4Vbeta8+ T cells but not of CD8Vbeta8+ T cells. SEB-promoted thymic deletion is not abolished by ISO; however, a rapid recovery of thymocyte numbers due to increased double-positive (DP) CD4+ CD8+ thymocyte proliferation was clearly observed in ISO-treated, SEB-injected mice but not in controls (untreated SEB-injected mice). It was also found that ISO inhibits the early SEB-induced cell proliferation (i.e., that found 12 h after SEB injection), accelerating the clonal anergy usually observed 3 days after SEB injection. Inhibition of T-cell proliferation by the NO donor does not appear to be due to inhibition of cytokine production. These results show that NO interferes with apoptosis and facilitates thymic proliferation of DP thymocytes, although it inhibits peripheral T-cell proliferation.

This article has been cited by other articles:

• Mahidhara, R. S., Hoffman, R. A., Huang, S., Wolf-Johnston, A., Vodovotz, Y., Simmons, R. L., Billiar, T. R. (2003). Nitric oxide-mediated inhibition of caspase-dependent T lymphocyte proliferation. J. Leukoc. Biol. 74: 403-411 [Abstract] [Full Text]  
• Blesson, S., Thiery, J., Gaudin, C., Stancou, R., Kolb, J.-P., Moreau, J.-L., Theze, J., Mami-Chouaib, F., Chouaib, S. (2002). Analysis of the mechanisms of human cytotoxic T lymphocyte response inhibition by NO. Int Immunol 14: 1169-1178 [Abstract] [Full Text]  
• Rachlis, A., Watson, J. L., Lu, J., McKay, D. M. (2002). Nitric oxide reduces bacterial superantigen-immune cell activation and consequent epithelial abnormalities. J. Leukoc. Biol. 72: 339-346 [Abstract] [Full Text]  
• McKay, D. M., Lu, J., Jedrzkiewicz, S., Ho, W., Sharkey, K. A. (1999). Nitric Oxide Participates in the Recovery of Normal Jejunal Epithelial Ion Transport Following Exposure to the Superantigen, Staphylococcus aureus Enterotoxin B. J. Immunol. 163: 4519-4526 [Abstract] [Full Text]  
• Virág, L., Haskó, G., Salzman, A. L., Szabó, C. (1998). NADPH Diaphorase Histochemistry Detects Inducible Nitric Oxide Synthetase Activity in the Thymus of Naive and Staphylococcal Enterotoxin B-stimulated Mice. J. Histochem. Cytochem. 46: 787-792 [Abstract] [Full Text]  
• Mutunga, M., Preston, P. M., Sumption, K. J. (1998). Nitric Oxide is Produced by Cowdria ruminantium-Infected Bovine Pulmonary Endothelial Cells In Vitro and Is Stimulated by Gamma Interferon. Infect. Immun. 66: 2115-2121 [Abstract] [Full Text]