Department of Orthopaedic Surgery and Rehabilitation, Loyola University Medical Center, 2160 South 1st Avenue, Maywood, IL 60153, USA.
J Bone Joint Surg Am. 2011 Apr 20;93(8):739-49. doi: 10.2106/JBJS.J.00318.
Alcohol is a known modulator of the immune system and host-defense response. Alcohol abuse is common in trauma patients, although the influence of alcohol intoxication on the inflammatory response following major orthopaedic injury remains unknown. The aim of this investigation was to examine the influence of binge alcohol exposure on biomarkers of the systemic inflammatory response following bilateral traumatic femoral fracture in a rodent model.
Ninety-two Sprague-Dawley rats were administered intraperitoneal injections of either saline solution or alcohol for three days. These animals then underwent a sham procedure or bilateral femoral intramedullary pinning and mid-diaphyseal closed fracture via blunt guillotine. The animals were killed at specific time points after the injury. Serum and lung tissue were collected, and twenty-five inflammatory markers were analyzed by immunoassay. Histological sections of lung tissue were evaluated by a board-certified pathologist.
Bilateral femoral fracture significantly (p < 0.05) increased multiple serum biomarkers of inflammation. Binge alcohol treatment prior to injury significantly suppressed the increase in serum levels of interleukin (IL)-6, white blood cells, IL-2, IL-10, and C-reactive protein after the fracture. However, alcohol-treated animals were found to have increased pulmonary levels of IL-6, IL-1β, IL-2, and macrophage inflammatory protein-1α following bilateral femoral fracture. In addition, lung tissue harvested following alcohol treatment and injury demonstrated increased pathologic changes, including parenchymal, alveolar, and peribronchial leukocyte infiltration and significantly elevated pulmonary wet-to-dry ratio, indicative of pulmonary edema.
Our results indicate that acute alcohol intake prior to bilateral femoral fracture with fixation in rats modulates the inflammatory response after injury in a tissue-dependent manner. Although serum biomarkers of inflammation were suppressed in alcohol-treated animals following injury, several measures of pulmonary inflammation including cytokine levels, histological changes, and findings of pulmonary edema were significantly increased following fracture with the presence of alcohol.
酒精是免疫系统和宿主防御反应的已知调节剂。创伤患者中常存在酒精滥用的情况，尽管酒精中毒对重大骨科损伤后炎症反应的影响尚不清楚。本研究旨在检查在创伤性双侧股骨骨折的啮齿动物模型中，急性酒精暴露对全身炎症反应生物标志物的影响。
92 只 Sprague-Dawley 大鼠接受腹腔注射生理盐水或酒精 3 天。这些动物随后接受假手术或双侧股骨髓内针固定和中干闭合性骨折的钝性断头台手术。在损伤后特定时间点处死动物。收集血清和肺组织，并通过免疫测定分析 25 种炎症标志物。由经过委员会认证的病理学家评估肺组织的组织学切片。
双侧股骨骨折显著（p < 0.05）增加了多种血清炎症标志物。损伤前急性酒精处理显著抑制了骨折后血清中白细胞介素（IL）-6、白细胞、IL-2、IL-10 和 C 反应蛋白水平的升高。然而，在双侧股骨骨折后，发现酒精处理的动物肺组织中 IL-6、IL-1β、IL-2 和巨噬细胞炎症蛋白-1α 的水平升高。此外，在接受酒精治疗和损伤后采集的肺组织显示出更多的病理变化，包括实质、肺泡和支气管周围白细胞浸润，以及显著升高的肺湿重/干重比，表明肺水肿。
我们的结果表明，在大鼠双侧股骨骨折固定前急性酒精摄入以组织依赖性方式调节损伤后的炎症反应。尽管在损伤后酒精处理的动物血清炎症标志物受到抑制，但在骨折存在酒精的情况下，几项肺炎症指标，包括细胞因子水平、组织学变化和肺水肿发现，均显著增加。
