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(+) Vbeta8(+) 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.