REGULATION OF THE POSTBURN WOUND INFLAMMATORY RESPONSE BY γδ T-CELLS

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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 γδ 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 γδ T-cell receptor-deficient (δ 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-α (TNF-α) and monocyte chemoattractant protein 1 levels. In WT mice, the numbers of infiltrating cells were similar between nonburn wounds and burn wounds. In contrast, δTCR−/−mice displayed a 6-fold reduction in the cellular infiltrate. Burn injury in WT mice caused a marked increase in burn wound TNF-α, monocyte chemoattractant protein 1, and interleukin 6 content as compared with nonburn wounds, whereas in δ TCR−/−mice, the burn-induced increase of TNF-α and interleukin 6 was not observed. The wound cell infiltrate at 3 days postinjury was devoid of γδ 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 γδ T-cells are important in the recruitment of inflammatory cells and regulation of the inflammatory response at the wound site after thermal injury.