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Sterile post-traumatic immunosuppression

机译:无菌创伤后免疫抑制

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摘要

After major trauma, the human immune system initiates a series of inflammatory events at the injury site that is later followed by suppression of local inflammation favoring the repair and remodeling of the damaged tissues. This local immune response involves complex interactions between resident cells such as macrophages and dendritic cells, soluble mediators such as cytokines and chemokines, and recruited cells such as neutrophils, monocytes and mesenchymal stromal cells. If of sufficient magnitude, these initial immune responses nevertheless have systemic consequences resulting in a state called post-traumatic immunosuppression (PTI). However, controversy exists regarding the exact immunological changes occurring in systemic compartments triggered by these local immune responses. PTI is one of the leading causes of post-surgical mortality and makes patients vulnerable to hospital-acquired infections, multiple organ failure and many other complications. In addition, hemorrhage, blood transfusion, immunesenescence and immunosuppressant drugs aggravate PTI. PTI has been intensively studied, but published results are frequently cloudy. The purpose of this review is to focus on the contributions made by different responsive modalities to immunosuppression following sterile trauma and to try to integrate these into an overall scheme of PTI.
机译:重大创伤后,人体免疫系统会在受伤部位引发一系列炎症事件,随后抑制局部炎症,从而促进受损组织的修复和重塑。这种局部免疫反应涉及常驻细胞(例如巨噬细胞和树突状细胞),可溶性介体(例如细胞因子和趋化因子)和募集的细胞(例如中性粒细胞,单核细胞和间充质基质细胞)之间的复杂相互作用。如果足够大,这些初始免疫反应仍然会导致全身性后果,导致称为创伤后免疫抑制(PTI)的状态。然而,关于由这些局部免疫反应触发的系统性区室中发生的确切免疫学变化存在争议。 PTI是术后死亡率的主要原因之一,使患者容易受到医院获得的感染,多器官功能衰竭和许多其他并发症的影响。此外,出血,输血,免疫衰老和免疫抑制剂药物加重了PTI。对PTI进行了深入研究,但已发表的结果经常是模糊的。这篇综述的目的是集中于无菌创伤后不同反应方式对免疫抑制的贡献,并试图将其整合到PTI的整体方案中。

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