Hypercapnic Conditions After Experimental Blunt Chest Trauma Increase Efferocytosis of Alveolar Macrophages and Reduce Local Inflammation
Hypercapnic Conditions After Experimental Blunt Chest Trauma Increase Efferocytosis of Alveolar Macrophages and Reduce Local Inflammation
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DOI：
10.1097/shk.0000000000000813
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发表时间：
2017-07
期刊：
影响因子：
3.1
通讯作者：
Annette Palmer;Michael S. J. Eichner;Anne Rittlinger;Daniel H. Seitz;F. Gebhard;M. Huber-Lang;Ulrike Niesler
中科院分区：
文献类型：
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作者：
Annette Palmer;Michael S. J. Eichner;Anne Rittlinger;Daniel H. Seitz;F. Gebhard;M. Huber-Lang;Ulrike Niesler
钝性胸部创伤可引起严重的局部和全身炎症改变，并在肺内积聚凋亡的多形粒细胞（aPMN），随后经常发生细菌感染。肺泡巨噬细胞（AM）是其清除的主要参与者之一。然而，很少有人知道有关的AM吞噬细胞和吞噬活动的调节和影响因素。在这种情况下，我们研究了受损的气体交换对AM活性的影响。雄性大鼠进行钝性胸部创伤或假手术，aPMN或大肠杆菌（E。coli）。随后，通过分析在三个时间点从支气管肺泡灌洗液中获得的AM来评估巨噬细胞和吞噬细胞活性。为了确定AM的吞噬细胞和吞噬细胞活性是否受到气体浓度变化的影响，AM在体外经受缺氧和高碳酸条件。创伤显著上调AM摄取E的能力。大肠杆菌感染后24小时开始，而aPMN摄取率几乎保持不变。在体外，AM对高碳酸血症条件的反应是通过增强与抗炎细胞因子释放增加相关的红细胞增多。此外，创伤后AM的吞噬作用和促炎反应似乎受损。与此相反，缺氧条件下显示AM没有调节作用。结论：钝性胸部创伤可增强AM的吞噬活性。另一方面，肺中的高碳酸血症状况可能显著有助于aPMN的清除。必须正确评估CO2在临床环境中的应用，平衡CO2的益处和细菌清除受损的不利影响。
ABSTRACT Blunt chest trauma induces severe local and systemic inflammatory alterations and an accumulation of apoptotic polymorphonuclear granulocytes (aPMN) in the lungs, frequently followed by bacterial infection. Alveolar macrophages (AM) represent one of the main actors for their clearance. However, little is known regarding regulatory and influencing factors of AM efferocytic and phagocytic activities. In this context, we investigated the influence of impaired gas exchange on AM activity. Male rats underwent blunt chest trauma or sham procedure and aPMN or Escherichia coli (E. coli) were instilled. Subsequently, the efferocytic and phagocytic activities were assessed by analyzing AM obtained from bronchoalveolar lavage fluids at three time points. To determine whether efferocytic and phagocytic activities of AM are affected by shifting gas concentrations, AM were subjected in vitro to hypoxic and hypercapnic conditions. Trauma significantly upregulated the capacity of AM to ingest E. coli starting 24 h after trauma, whereas the aPMN uptake rate remained virtually unchanged. In vitro, AM reacted to hypercapnic conditions by enhanced efferocytosis associated with increased release of anti-inflammatory cytokines. Additionally, phagocytosis and the pro-inflammatory reaction of AM after trauma appeared to be impaired. In contrast, hypoxic conditions displayed no regulatory effect on AM. In conclusion, blunt chest trauma enhances phagocytic activity of AM. On the other hand, hypercapnic conditions in the lungs may significantly contribute to the clearance of aPMN. The application of CO2 in clinical settings must be properly assessed, with the benefits of CO2 balanced against the detrimental effects of impaired bacterial clearance.