title: Increased T cell chemotaxis response to Staphylococcus enterotoxin B mediated human endothelial cell damage in vitro.
abstract: 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.
authors.affiliation: Department of Guangzhou Institute of Respiratory Disease, First Affiliated Hospital, Guangzhou Medical College, Guangzhou, China1st Affiliated Hospital of JINAN University, Guangzhou, ChinaDepartment of Guangzhou Research Institute of Snake Venom, Guangzhou, China.
authors.forename: Z
authors.initials: Z
authors.lastname: Xiao
authors.affiliation: Department of Guangzhou Institute of Respiratory Disease, First Affiliated Hospital, Guangzhou Medical College, Guangzhou, China1st Affiliated Hospital of JINAN University, Guangzhou, ChinaDepartment of Guangzhou Research Institute of Snake Venom, Guangzhou, China.
authors.forename: L
authors.initials: L
authors.lastname: Wu
authors.affiliation: Department of Guangzhou Institute of Respiratory Disease, First Affiliated Hospital, Guangzhou Medical College, Guangzhou, China1st Affiliated Hospital of JINAN University, Guangzhou, ChinaDepartment of Guangzhou Research Institute of Snake Venom, Guangzhou, China.
authors.forename: H
authors.initials: H
authors.lastname: Mo
authors.affiliation: Department of Guangzhou Institute of Respiratory Disease, First Affiliated Hospital, Guangzhou Medical College, Guangzhou, China1st Affiliated Hospital of JINAN University, Guangzhou, ChinaDepartment of Guangzhou Research Institute of Snake Venom, Guangzhou, China.
authors.forename: T
authors.initials: T
authors.lastname: Kong
mesh_terms: D002470:Cell Survival; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000235:genetics / Q000276:immunology; D054405:Chemokine CCL3 / Q000235:genetics / Q000276:immunology; D018946:Chemokine CCL5 / Q000235:genetics / Q000276:immunology; D002634:Chemotaxis, Leukocyte / Q000187:drug effects*; D018920:Coculture Techniques; D042783:Endothelial Cells / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D004768:Enterotoxins / Q000494:pharmacology*; D005786:Gene Expression Regulation; D006801:Humans; D008213:Lymphocyte Activation / Q000187:drug effects; D060888:Real-Time Polymerase Chain Reaction; D054390:Receptors, CCR2 / Q000235:genetics / Q000276:immunology; D054397:Receptors, CCR3 / Q000235:genetics / Q000276:immunology; D019713:Receptors, CCR5 / Q000235:genetics / Q000276:immunology; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000187:drug effects* / Q000276:immunology / Q000473:pathology
chemical_list: C111835:CCL2 protein, human; C515334:CCR2 protein, human; C515350:CCR3 protein, human; C584933:CCR5 protein, human; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D018946:Chemokine CCL5; D004768:Enterotoxins; D054390:Receptors, CCR2; D054397:Receptors, CCR3; D019713:Receptors, CCR5; C031818:enterotoxin B, staphylococcal