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

Abstract

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). To determine whether the two superantigens interact to cause an enhancement of biological activity in human peripheral blood mononuclear cells (PBMCs). PBMCs from nine healthy donors were stimulated with TSST-1 or SEA, either alone or in combination at their minimum effective concentrations. In vitro study. 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 [(3)H]-thymidine incorporation. PBMC culture supernatants were assayed for the presence of tumour necrosis factor-alpha (TNFα), interleukin (IL)-1β and IL-6 by ELISA. 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. 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.