Interaction of staphylococcal toxic shock syndrome toxin-1 and enterotoxin A on T cell proliferation and TNFα secretion in human blood mononuclear cells

2Citations
Citations of this article
10Readers
Mendeley users who have this article in their library.

This article is free to access.

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). 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 through an enhanced effect of these superantigens on T cell activation and TNF secretion.

Cite

CITATION STYLE

APA

De Boer, M. L., Kum, W. W. S., & Chow, A. W. (1999). Interaction of staphylococcal toxic shock syndrome toxin-1 and enterotoxin A on T cell proliferation and TNFα secretion in human blood mononuclear cells. Canadian Journal of Infectious Diseases, 10(6), 403–409. https://doi.org/10.1155/1999/234876

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free