Regulatory T Cells Modulate Staphylococcal Enterotoxin B-Induced Effector T-Cell Activation and Acceleration of Colitis

Abstract

ABSTRACT Oral administration of bacterial superantigen Staphylococcus aureus enterotoxin B (SEB) activates mucosal T cells but does not cause mucosal inflammation. We examined the effect of oral SEB on the development of mucosal inflammation in mice in the absence of regulatory T (Treg) cells. SCID mice were fed SEB 3 and 7 days after reconstitution with CD4 + CD45RB high or CD4 + CD45RB high plus CD4 + CD45RB low T cells. Mice were sacrificed at different time points to examine changes in tissue damage and in T-cell phenotypes. Feeding SEB failed to produce any clinical effect on SCID mice reconstituted with CD4 + CD45RB high and CD4 + CD45RB low T cells, but feeding SEB accelerated the development of colitis in SCID mice reconstituted with CD4 + CD45RB high T cells alone. The latter was associated with an increase in the number of CD4 + Vβ8 + T cells expressing CD69 and a significantly lower number of CD4 + CD25 + Foxp3 + T cells. These changes were not observed in SCID mice reconstituted with both CD45RB high and CD45RB low T cells. In addition, SEB impaired the development of Treg cells in the SCID mice reconstituted with CD4 + CD45RB high T cells alone but had no direct effect on Treg cells. In the absence of Treg cells, feeding SEB induced activation of mucosal T cells and accelerated the development of colitis. This suggests that Treg cells prevent SEB-induced mucosal inflammation through modulation of SEB-induced T-cell activation.