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Increased T Cell Chemotaxis Response to Staphylococcus Enterotoxin B Mediated Human Endothelial Cell Damage In Vitro
Author(s) -
Xiao Z.,
Wu L.,
Mo H.,
Kong T.
Publication year - 2012
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2011.02638.x
Subject(s) - chemokine , chemotaxis , downregulation and upregulation , endothelial stem cell , microbiology and biotechnology , superantigen , immunology , chemokine receptor , cytokine , ccl5 , t cell , endothelium , cell , inflammation , biology , chemistry , receptor , in vitro , immune system , il 2 receptor , endocrinology , biochemistry , genetics , gene
The severity of superantigen (SAg)‐mediated shock is associated with T cell infiltration in major organs [1, 2]. 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.