Daniel Tanjanika, Thobe Bjoern M, Chaudry Irshad H, Choudhry Mashkoor A, Hubbard William J, Schwacha Martin G
Center for Surgical Research, Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
Shock. 2007 Sep;28(3):278-83. doi: 10.1097/shk.0b013e318034264c.
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.
烧伤创面的愈合是患者从这种创伤形式中成功康复的关键组成部分。我们实验室之前的研究表明，γδT细胞通过产生生长因子在烧伤创面愈合中起重要作用。尽管如此，这些细胞在烧伤创面炎症中的作用仍不清楚。为了研究这一点，将野生型（WT）和γδT细胞受体缺陷型（δTCR）C57BL/6雄性小鼠进行烧伤或假手术。通过在受伤小鼠的烧伤部位下方或假手术小鼠的未受伤皮肤下方植入聚乙烯醇海绵来收集创面细胞。在受伤后3天，收集浸润细胞、创面渗出液和皮肤进行分析。烧伤显著增加了皮肤肿瘤坏死因子-α（TNF-α）和单核细胞趋化蛋白1水平。在WT小鼠中，非烧伤创面和烧伤创面的浸润细胞数量相似。相比之下，δTCR小鼠的细胞浸润减少了6倍。与非烧伤创面相比，WT小鼠的烧伤导致烧伤创面TNF-α、单核细胞趋化蛋白1和白细胞介素6含量显著增加，而在δTCR小鼠中，未观察到烧伤诱导的TNF-α和白细胞介素6增加。受伤后3天，WT小鼠创面的细胞浸润中没有γδT细胞。它主要起源于髓系，表达高水平的CD11b和F4/80。总之，这些发现表明，驻留的γδT细胞在热损伤后创面部位炎症细胞的募集和炎症反应的调节中起重要作用。
