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首页> 外文期刊>Shock: Molecular, cellular, and systemic pathobiological aspects and therapeutic approaches = The official journal of the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies >Does burn wound excision after thermal injury attenuate subsequent macrophage hyperactivity and immunosuppression?
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Does burn wound excision after thermal injury attenuate subsequent macrophage hyperactivity and immunosuppression?

机译：燃烧热受伤后伤口切除吗减弱随后巨噬细胞过度活跃免疫抑制?

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摘要

Studies have shown that cell mediated immunity is suppressed markedly following thermal injury. Macrophages and the activation of an inflammatory cascade that includes interleukin (IL)-1, IL-6, tumor necrosis factor-alpha (TNFalpha) and PGE2 have been implicated as causative factors. Burn wound excision and grafting is a common clinical practice that decreases patient morbidity and mortality. It is not known, however, if the salutary effects of this procedure are related to modulation of macrophage activity post-burn. Therefore, C57BL/6 female mice were subjected to a third-degree scald burn covering 25% of their total body surface area followed by complete excision and allografting of the injury site at 8, 24, or 72 h post-burn. Splenic macrophage function was assessed 7 days post-burn. Thermal injury without burn excision and grafting significantly increased macrophage TNFalpha, IL-6, nitric oxide, and PGE2 production in response to lipopolysaccharide stimulation, whereas IL-1beta production was not increased. Burn wound excision and grafting normalized TNFalpha production to sham levels, independent of when post-burn the procedure was conducted. In contrast, the elevated production of other inflammatory mediators (IL-1beta, IL-6, nitric oxide, PGE2) post-burn was unaffected by burn wound excision and grafting. Moreover, splenic T-lymphocyte proliferation was also suppressed at 7 days post-burn and was not improved by burn wound excision and grafting. These results, therefore, suggest that the beneficial effects of burn wound excision and grafting are likely to be related to the normalization of macrophage TNFalpha production as well as the maintenance of skin barrier function.
机译：研究表明,细胞介导免疫显著抑制热损伤。巨噬细胞的激活和炎症级联,包括白介素(IL) 1、IL - 6,肿瘤坏死因子-α(TNFalpha)和PGE2牵扯诱发因素。伤口切除和移植是一种常见的临床实践,降低患者发病率和死亡率。这个过程相关的有益的影响调制烧伤患者巨噬细胞的活动。因此,C57BL / 6雌性老鼠受到一个三度烫伤烧伤覆盖25%的全身面积其次是完整的切除和同种异体移植物损伤部位8日,24日或72 h烧伤后。函数评估烧伤后7天。伤害没有燃烧切除和移植显著提高巨噬细胞TNFalpha,il - 6、一氧化氮和产生PGE2对脂多糖刺激,而IL-1beta产量没有增加。烧伤创面切除和移植规范化TNFalpha生产假的水平,独立当烧伤后的程序进行。相反,提高生产炎症介质(IL-1beta, il - 6,氮氧化,PGE2)烧伤后被燃烧的影响伤口切除和移植。t淋巴球增生也被抑制烧伤后7天,也提高了燃烧伤口切除和移植。因此,建议的有利影响烧伤创面切除和移植是可能相关巨噬细胞的正常化TNFalpha生产以及维护皮肤屏障功能。

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