Effects of acute ethanol exposure on the early inflammatory response after excisional injury
Effects of acute ethanol exposure on the early inflammatory response after excisional injury
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DOI：
10.1111/j.1530-0277.2006.00307.x
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发表时间：
2007-02-01
影响因子：
3.2
通讯作者：
Kovacs, Elizabeth J.
中科院分区：
文献类型：
--
作者：
Fitzgerald, Daniel J.;Radek, Katherine A.;Kovacs, Elizabeth J.
背景：超过一半的创伤相关伤害与饮酒有关。已知与未接触乙醇的患者相比，这些患者在受伤后表现出更高的死亡率和发病率。我们实验室的研究表明，乙醇暴露会损害真皮伤口后的再上皮化和血管生成，并且伤口愈合的早期炎症阶段可能会影响以后的反应，因此我们选择在真皮切除伤口后检查皮肤中的中性粒细胞浸润以及趋化因子和促炎细胞因子水平。方法：BALB/c 小鼠按设计剂量给予乙醇 治疗后 30 分钟将血液酒精浓度提高至 100 至 120 mg/dL。然后对小鼠进行全层切除伤口。在受伤后 24 小时内收集乙醇和盐水处理小鼠的伤口，以评估中性粒细胞浸润和髓过氧化物酶 (MPO) 活性、中性粒细胞趋化巨噬细胞炎症蛋白 2 (MIP-2) 和 KC 水平，以及促炎细胞因子白细胞介素 1 β (IL-1 β) 和肿瘤坏死因子 α (TNF α) 水平。结果：在受伤后 12 和 24 小时，与媒介物处理的动物的伤口相比，暴露于乙醇的小鼠伤口中的 MPO 显着减少。尽管如此，伤口的组织学检查并未显示两组之间中性粒细胞浸润的差异。与对照小鼠的伤口相比，在受伤后 12 小时观察到的 MIP-2 和 KC 峰值水平在乙醇处理小鼠的伤口中分别降低了 32% 和 45%。还评估了 TNF α 和 IL-1 β（MIP-2 和 KC 的有效诱导剂，以及中性粒细胞活化）的水平。受伤后两组的 TNF α 水平均未升高。然而，在经过乙醇处理的小鼠伤口中，IL-1β 在受伤后 6 小时的峰值水平显着降低，比对照组伤口低 58%。结论：这些研究表明，在受伤前给予乙醇的小鼠中，早期真皮炎症反应（包括 MPO 活性、MIP-2、KC 和 IL-1β 的产生）受到损害，这也可能对伤口愈合的后期产生不利影响。
Background: Alcohol consumption is involved in over half of all trauma-related injuries. These patients are known to exhibit a higher incidence of mortality and morbidity following injury compared with patients not exposed to ethanol. As studies from our laboratory demonstrated that ethanol exposure impairs re-epithelialization and angiogenesis after dermal wounding and because the earlier inflammatory phase of wound healing is likely to influence later responses, we chose to examine neutrophil infiltration and chemokine and proinflammatory cytokine levels in the skin following administration of a dermal excisional wound.Methods: BALB/c mice were given ethanol at a dose designed to increase blood alcohol concentration to 100 to 120 mg/dL at 30 minutes after treatment. Mice were then subjected to a full-thickness excisional wound. Wounds from ethanol and saline-treated mice were collected within the first 24 hours postinjury to assess neutrophil infiltration and myeloperoxidase (MPO) activity, neutrophil chemoattractant macrophage inflammatory protein-2 (MIP-2) and KC levels, and proinflammatory cytokine interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha) levels.Results: At 12 and 24 hours after injury, MPO in wounds from ethanol-exposed mice was significantly reduced compared with wounds from vehicle-treated animals. Despite this, histological examination of wounds did not reveal a difference in neutrophil infiltration between the 2 groups. Peak levels of MIP-2 and KC observed at 12 hours postinjury were decreased in wounds from ethanol-treated mice by 32 and 45%, respectively, relative to wounds from control mice. Levels of TNF alpha and IL-1 beta (potent inducers of MIP-2 and KC, as well as neutrophil activation) were also assessed. Levels of TNF alpha were not elevated in either group after injury. However, IL-1 beta demonstrated significantly lower peak levels at 6 hours postinjury in wounds from ethanol-treated mice, 58% less than wounds from controls.Conclusions: These studies reveal that early dermal inflammatory responses including MPO activity, production of MIP-2, KC, and IL-1 beta are impaired in mice given ethanol before injury, which may also have detrimental affects on later stages of wound healing.