Interaction of staphylococcal toxic shock syndrome toxin-1 and enterotoxin A on T-cell proliferation and TNF<font face=\'symbol\'>a</font> secretion in human blood mononuclear cells, Pulsus Group Inc
CANADIAN JOURNAL OF INFECTIOUS DISEASES & MEDICAL MICROBIOLOGY
Association of Medical Microbiology & Infectious Diseases (AMMI Canada)

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Original Article November/December 1999, Volume 10 Issue 6: 403-409
 

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

ML De Boer | WWS Kum | AW Chow

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 (TNFa), interleukin (IL)-1b 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 TNFa 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.


Cytokines | Mitogenic response | Staphylococcal enterotoxin A | Toxic shock syndrome toxin-1
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