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Canadian Journal of Infectious Diseases
Volume 10, Issue 6, Pages 403-409
http://dx.doi.org/10.1155/1999/234876
Original Article

Interaction of Staphylococcal Toxic Shock Syndrome Toxin-1 and Enterotoxin A on T Cell Proliferation and TNFα Secretion in Human Blood Mononuclear Cells

Monica L De Boer,1 Winnie WS Kum,1 and Anthony W Chow1,2,3

1Division of Infectious Diseases, Department of Medicine, University of British Columbia the Canadian Bacterial Diseases Network, Vancouver, British Columbia, Canada
2Department of Microbiology and Immunology, University of British Columbia the Canadian Bacterial Diseases Network, Vancouver, British Columbia, Canada
3Vancouver Hospital and Health Sciences Centre, Vancouver, British Columbia, Canada

Received 31 August 1998; Accepted 25 February 1999

Copyright © 1999 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

BACKGROUND: The majority of menstrual toxic shock syndrome (MTSS) cases are caused by a single clone of Staphylococcus aureus that produces both toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin A (SEA).

OBJECTIVE: To determine whether the two superantigens interact to cause an enhancement of biological activity in human peripheral blood mononuclear cells (PBMCs).

DESIGN: PBMCs from nine healthy donors were stimulated with TSST-1 or SEA, either alone or in combination at their minimum effective concentrations.

SETTING: In vitro study.

INTERVENTIONS: Human PBMCs were stimulated in vitro with TSST-1 (1 pg/mL), SEA (0.1 pg/mL) or combination for 20 to 72 h. Mitogenic response was determined by [3H]-thymidine incorporation. PBMC culture supernatants were assayed for the presence of tumour necrosis factor-alpha (TNFα), interleukin (IL)-1β and IL-6 by ELISA.

MAIN RESULTS: The combination of TSST-1 and SEA induced significantly greater mitogenesis in human PBMCs compared with either toxin alone (P<0.05, paired Student’s t test, two-tailed). Similarly, the production of TNFα in culture supernatants was significantly greater in the combination of TSST-1 and SEA compared with either TSST-1 or SEA alone (P<0.05). In contrast, no enhancement in the levels IL-1 or IL-6 was observed.

CONCLUSIONS: These data suggest that the co-production of TSST-1 and SEA by S aureus may provide some biological advantage to the organism throughs an enhanced effect of these superantigens on T cell activation and TNF secretion.