Increased T cell chemotaxis response to Staphylococcus enterotoxin B mediated human endothelial cell damage in vitro

The severity of superantigen (SAg)-mediated shock is associated with T cell infiltration in major organs. We postulated that endothelial cell inflammation and damage in sepsis might be mediated by chemotaxis and adherence of SAg-activated T cells of vascular endothelium. We therefore investigate whether staphylococcal enterotoxin B (SEB) could modulate chemokine receptors expression on T cells as well as cytokine release, and then we examined the up-modulation of chemokine-associated affect on T cell-mediated damage of endothelial cells. We consistently observed that SEB could upregulate expression of CCR5 on T cells and induce a panel of cytokines release from T cell, the latter could further induce increased release of chemokine such as MCP-1, MIP-1α and RANTES from human pulmonary artery endothelial cell (HPAEC). Both upregulation of CCR5 on SEB-activated T cell and increased release of chemokine from HPAEC contribute to higher chemoattraction and adherence of T cell to HPAEC and ultimately led to more extensive endothelial damage. (These data suggest that T cell migration and acute inflammatory response in bacterial SAg-mediated shock maybe explained partly by upregulation of chemotaxis of T cell of endothelium.) Revised as following: Our results demonstrate that upregulation of chemotaxis of T cell of endothelium is SEB specific, and this mechanism could account in part for T cell migration and acute inflammatory response in bacterial SAg-mediated shock.