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.