Hypercapnic Conditions After Experimental Blunt Chest Trauma Increase Efferocytosis of Alveolar Macrophages and Reduce Local Inflammation

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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.

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