INSERM, U1016, Institut Cochin, Paris, France; CNRS, UMR 8104, Paris, France; Université Paris Descartes, Sorbonne Paris Cité, Paris, France.
AstraZeneca, Precision Medicine & Genomics, RIA Companion Diagnostics Unit, Sweden.
Biomed J. 2017 Dec;40(6):305-312. doi: 10.1016/j.bj.2017.09.004. Epub 2017 Dec 26.
In the normal non-diseased lung, various macrophage populations maintain homeostasis and sterility by ingesting and clearing inhaled particulates, pathogens and apoptotic cells from the local environment. This process of phagocytosis leads to the degradation of the internalized material, coordinated induction of gene expression, antigen presentation and cytokine production, implicating phagocytosis as a central regulator of innate immunity. Phagocytosis is extremely efficient and any perturbation of this function is deleterious. In inflammatory lung diseases such as chronic obstructive pulmonary disease (COPD), despite their increased numbers, macrophages demonstrate significantly reduced phagocytic capacity of bacteria and apoptotic cells. This defect could play a role in dysbiosis of the lung microbiome contributing to disease pathophysiology. In this review, we will discuss lung macrophages, describe phagocytosis and its related downstream processes and the reported phagocytosis defects in COPD. Finally, we will briefly examine current strategies that focus on restoring the phagocytic capabilities of lung macrophages that may have utility in COPD.
在正常的非病变肺部中，各种巨噬细胞群通过吞噬和清除吸入的颗粒物、病原体和凋亡细胞来维持局部环境的内稳态和无菌状态。这个吞噬过程导致内化物质的降解、协调诱导基因表达、抗原呈递和细胞因子产生，表明吞噬作用是先天免疫的核心调节剂。吞噬作用非常高效，任何对这种功能的干扰都是有害的。在炎症性肺部疾病（如慢性阻塞性肺疾病，COPD）中，尽管巨噬细胞数量增加，但它们对细菌和凋亡细胞的吞噬能力明显降低。这种缺陷可能在导致疾病病理生理学的肺部微生物组失调中发挥作用。在这篇综述中，我们将讨论肺巨噬细胞，描述吞噬作用及其相关的下游过程以及 COPD 中报道的吞噬作用缺陷。最后，我们将简要探讨目前专注于恢复肺巨噬细胞吞噬能力的策略，这些策略可能在 COPD 中具有应用价值。
