title: The role of gammadelta T cells in the regulation of neutrophil-mediated tissue damage after thermal injury.
abstract: Thermal injury induces an inflammatory response that contributes to the development of secondary tissue damage. Neutrophil recruitment and activation are in part responsible for this tissue damage. Although gammadelta T cells have been shown to regulate the inflammatory responses in tissues that are prone to neutrophil-mediated injury post-burn, their role in the induction of secondary tissue injury post-burn remains unknown. To study this, gammadelta T cell-deficient (gammadelta TCR-/-) and wild-type (WT) mice were subjected to thermal injury or sham procedure, and tissue samples were isolated 1-24 h thereafter. Burn injury induced neutrophil accumulation in the lung and small intestines of WT mice at 1-3 h post-injury. No such increase in neutrophil tissue content was observed in gammadelta TCR-/- mice. An increase in tissue wet/dry weight ratios was also observed in these organs at 3 h post-burn in WT but not in gammadelta TCR-/- mice. A parallel increase in plasma and small intestine levels of the chemokines macrophage-inflammatory protein-1beta (chemokine ligand 4) and keratinocyte-derived chemokine (CXC chemokine ligand 1) were observed in injured WT mice but not in injured gammadelta TCR-/- mice. Increased activation (CD120b expression) of the circulating gammadelta T cell population was also observed at 3 h post-burn in WT mice. These results indicate the gammadelta T cells, through the production of chemokines, play a central role in the initiation of neutrophil-mediated tissue damage post-burn.
authors.affiliation: Center for Surgical Research, Department of Surgery, G094 Volker Hall, 1670 University Blvd., Birmingham, AL 35294-0019, USA.
authors.forename: Balazs
authors.initials: B
authors.lastname: Toth
authors.forename: Michelle
authors.initials: M
authors.lastname: Alexander
authors.forename: TanJanika
authors.initials: T
authors.lastname: Daniel
authors.forename: Irshad H
authors.initials: IH
authors.lastname: Chaudry
authors.forename: William J
authors.initials: WJ
authors.lastname: Hubbard
authors.forename: Martin G
authors.initials: MG
authors.lastname: Schwacha
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000276:immunology; D002056:Burns / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D002455:Cell Division / Q000235:genetics / Q000276:immunology; D054407:Chemokine CCL4; D002634:Chemotaxis, Leukocyte / Q000235:genetics / Q000276:immunology; D007153:Immunologic Deficiency Syndromes / Q000235:genetics*; D007249:Inflammation / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D007421:Intestine, Small / Q000276:immunology / Q000503:physiopathology; D008168:Lung / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D019402:Macrophage Inflammatory Proteins / Q000276:immunology / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009504:Neutrophils / Q000276:immunology*; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000172:deficiency* / Q000235:genetics / Q000276:immunology*; D023062:Receptors, Interleukin-8A / Q000276:immunology; D018124:Receptors, Tumor Necrosis Factor / Q000276:immunology; D047889:Receptors, Tumor Necrosis Factor, Type II; D013601:T-Lymphocytes / Q000276:immunology*; D015854:Up-Regulation / Q000276:immunology
chemical_list: D015703:Antigens, CD; D054407:Chemokine CCL4; D019402:Macrophage Inflammatory Proteins; D016692:Receptors, Antigen, T-Cell, gamma-delta; D023062:Receptors, Interleukin-8A; D018124:Receptors, Tumor Necrosis Factor; D047889:Receptors, Tumor Necrosis Factor, Type II