Hu Parker J, Pittet Jean-Francois, Kerby Jeffrey D, Bosarge Patrick L, Wagener Brant M
Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama.
Department of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham, Birmingham, Alabama; and.
Am J Physiol Lung Cell Mol Physiol. 2017 Jul 1;313(1):L1-L15. doi: 10.1152/ajplung.00485.2016. Epub 2017 Apr 13.
Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Even when patients survive the initial insult, there is significant morbidity and mortality secondary to subsequent pulmonary edema, acute lung injury (ALI), and nosocomial pneumonia. Whereas the relationship between TBI and secondary pulmonary complications is recognized, little is known about the mechanistic interplay of the two phenomena. Changes in mental status secondary to acute brain injury certainly impair airway- and lung-protective mechanisms. However, clinical and translational evidence suggests that more specific neuronal and cellular mechanisms contribute to impaired systemic and lung immunity that increases the risk of TBI-mediated lung injury and infection. To better understand the cellular mechanisms of that immune impairment, we review here the current clinical data that support TBI-induced impairment of systemic and lung immunity. Furthermore, we also review the animal models that attempt to reproduce human TBI. Additionally, we examine the possible role of damage-associated molecular patterns, the chlolinergic anti-inflammatory pathway, and sex dimorphism in post-TBI ALI. In the last part of the review, we discuss current treatments and future pharmacological therapies, including fever control, tracheostomy, and corticosteroids, aimed to prevent and treat pulmonary edema, ALI, and nosocomial pneumonia after TBI.
创伤性脑损伤（TBI）是全球范围内导致死亡和发病的主要原因。即使患者在最初的损伤中幸存下来，随后也会因肺水肿、急性肺损伤（ALI）和医院获得性肺炎而出现显著的发病和死亡情况。虽然TBI与继发性肺部并发症之间的关系已为人所知，但对于这两种现象的机制相互作用却知之甚少。急性脑损伤继发的精神状态变化肯定会损害气道和肺部的保护机制。然而，临床和转化医学证据表明，更具体的神经元和细胞机制会导致全身和肺部免疫功能受损，从而增加TBI介导的肺损伤和感染风险。为了更好地理解这种免疫损伤的细胞机制，我们在此回顾支持TBI诱导全身和肺部免疫损伤的当前临床数据。此外，我们还回顾了试图重现人类TBI的动物模型。此外，我们研究了损伤相关分子模式、胆碱能抗炎途径和性别差异在TBI后ALI中的可能作用。在综述的最后部分，我们讨论了当前针对TBI后预防和治疗肺水肿、ALI和医院获得性肺炎的治疗方法及未来的药物治疗，包括体温控制、气管切开术和皮质类固醇。
