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首页> 外文期刊>Journal of orthopaedic trauma >The role of fracture-associated soft tissue injury in the induction of systemic inflammation and remote organ dysfunction after bilateral femur fracture.
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The role of fracture-associated soft tissue injury in the induction of systemic inflammation and remote organ dysfunction after bilateral femur fracture.

机译：骨折相关的软组织损伤在双侧股骨骨折后诱发全身性炎症和远端器官功能障碍中的作用。

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OBJECTIVES: The storage of preformed cytokines in soft tissue as well as the immunocompetence of adipocytes has been reported. We hypothesized that fracture-associated soft tissue injury plays a pivotal role in the induction of systemic inflammation and remote organ dysfunction after fracture. MATERIALS AND METHODS: Male C57/BL6 mice sustained either severe soft tissue injury to both thighs (STI), bilateral femur fracture with minimal soft tissue injury (Fx), or the combination of both (Fx+STI) and were euthanized 6 hours after injury. Serum cytokine concentrations were measured using the Luminex multiplexing platform, and serum ALT levels were measured with the Vitros 950 Chemistry System. Hepatic myeloperoxidase activity, a marker for polymorphonuclear cell infiltration, and hepatic IL-6 levels were determined using ELISA kits. Hepatic permeability changes were assessed via measurement of edema formation. RESULTS: STI as well as Fx both induced significantly elevated serum IL-6 and L-10 levels as compared with Sham animals (P 0.05). Further, serum IL-6 and IL-10 levels were significantly higher after STI as compared with Fx (P 0.05). Serum KC and MCP-1 levels were significantly elevated after STI but not after Fx (P 0.05). STI as well as Fx resulted in significantly increased serum ALT levels and hepatic polymorphonuclear cell infiltration. The combination of both injuries resulted in further increased systemic inflammatory mediators as well as marked liver inflammation and dysfunction represented by significantly elevated serum ALT levels, hepatic polymorphonuclear cell infiltration, hepatic IL-6 concentrations, and hepatic edema formation as compared with Sham animals (P 0.05). CONCLUSIONS: Although STI and Fx both induced a systemic inflammatory response, this was more pronounced after STI. However, the combination of both injuries (Fx+STI) was required to induce marked liver dysfunction. Our data indicate that fracture-associated soft tissue injury is a major contributor to thesystemic inflammatory response after bilateral femur fracture. This should be recognized especially in multiply injured patients, who are susceptible to systemic inflammation with remote organ dysfunction.
机译：目的：已经报道了预先形成的细胞因子在软组织中的存储以及脂肪细胞的免疫能力。我们假设与骨折相关的软组织损伤在骨折后诱发全身性炎症和远端器官功能障碍中起关键作用。材料与方法：雄性C57 / BL6小鼠要么对大腿（STI）造成严重的软组织损伤，要么将股骨骨折的软组织损伤降至最低（Fx），要么对二者进行联合治疗（Fx + STI），并在6小时后实施安乐死受伤。使用Luminex多路复用平台测量血清细胞因子浓度，并使用Vitros 950化学系统测量血清ALT水平。使用ELISA试剂盒测定了肝髓过氧化物酶活性，多形核细胞浸润的标志物和肝IL-6水平。肝通透性变化是通过测量水肿形成来评估的。结果：与假手术动物相比，STI和Fx均诱导血清IL-6和L-10水平显着升高（P <0.05）。此外，STI后的血清IL-6和IL-10水平明显高于Fx（P <0.05）。 STI后，血清KC和MCP-1水平显着升高，而Fx后则未升高（P <0.05）。 STI和Fx导致血清ALT水平和肝多形核细胞浸润明显增加。与假手术动物相比，这两种损伤的结合导致全身炎症介质的进一步增加，以及明显的肝脏炎症和功能障碍，表现为血清ALT水平明显升高，肝多形核细胞浸润，肝IL-6浓度和肝水肿形成（P <0.05）。结论：尽管STI和Fx均引起全身性炎症反应，但在STI后更为明显。但是，需要两种损伤的组合（Fx + STI）来诱发明显的肝功能障碍。我们的数据表明，与骨折相关的软组织损伤是双侧股骨骨折后全身炎症反应的主要因素。尤其是在多发伤的患者中，尤其是在易受全身器官功能异常的全身性炎症影响的患者中，这一点应得到认可。

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