title: Regulation of the postburn wound inflammatory response by gammadelta T-cells.
abstract: Healing of the burn injury site is a critical component of the patient's successful recovery from this form of trauma. Previous studies from our laboratory have demonstrated that gammadelta T-cells via the production of growth factors are important in burn wound healing. Nonetheless, the role of these cells in burn wound inflammation remains unknown. To study this, wild-type (WT) and gammadelta T-cell receptor-deficient (delta TCR) C57BL/6 male mice were subjected to burn injury or sham procedure. Wound cells were collected by implantation of polyvinyl alcohol sponges beneath the burn site in injured mice or beneath uninjured skin in sham mice. At 3 days after injury, infiltrating cells, wound fluid, and skin were collected for analysis. Burn injury markedly increased skin tumor necrosis factor-alpha (TNF-alpha) and monocyte chemoattractant protein 1 levels. In WT mice, the numbers of infiltrating cells were similar between nonburn wounds and burn wounds. In contrast, deltaTCRmice displayed a 6-fold reduction in the cellular infiltrate. Burn injury in WT mice caused a marked increase in burn wound TNF-alpha, monocyte chemoattractant protein 1, and interleukin 6 content as compared with nonburn wounds, whereas in delta TCRmice, the burn-induced increase of TNF-alpha and interleukin 6 was not observed. The wound cell infiltrate at 3 days postinjury was devoid of gammadelta T-cells in WT mice. It was predominately of myeloid origin expressing high levels of CD11b and F4/80. In conclusion, these findings suggest that resident gammadelta T-cells are important in the recruitment of inflammatory cells and regulation of the inflammatory response at the wound site after thermal injury.
authors.affiliation: Center for Surgical Research, Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
authors.forename: Tanjanika
authors.initials: T
authors.lastname: Daniel
authors.forename: Bjoern M
authors.initials: BM
authors.lastname: Thobe
authors.forename: Irshad H
authors.initials: IH
authors.lastname: Chaudry
authors.forename: Mashkoor A
authors.initials: MA
authors.lastname: Choudhry
authors.forename: William J
authors.initials: WJ
authors.lastname: Hubbard
authors.forename: Martin G
authors.initials: MG
authors.lastname: Schwacha
mesh_terms: D000818:Animals; D000943:Antigens, Differentiation / Q000096:biosynthesis; D002056:Burns / Q000473:pathology / Q000503:physiopathology*; D039481:CD11b Antigen / Q000096:biosynthesis; D017252:CD3 Complex / Q000096:biosynthesis; D018932:Chemokine CCL2 / Q000096:biosynthesis; D016207:Cytokines / Q000378:metabolism; D003872:Dermatitis / Q000276:immunology*; D015850:Interleukin-6 / Q000096:biosynthesis; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000502:physiology*; D012867:Skin / Q000378:metabolism; D016176:T-Lymphocyte Subsets / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D014945:Wound Healing / Q000502:physiology*
chemical_list: D000943:Antigens, Differentiation; D039481:CD11b Antigen; D017252:CD3 Complex; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D016207:Cytokines; D015850:Interleukin-6; D016692:Receptors, Antigen, T-Cell, gamma-delta; D014409:Tumor Necrosis Factor-alpha; C036763:monocyte-macrophage differentiation antigen