The role of lung macrophages in acute respiratory distress syndrome

Abstract

Acute respiratory distress syndrome (ARDS) is an acute and diffuse inflammatory lung injury in a short time, one of the common severe manifestations of the respiratory system that endangers human life and health. As an innate immune cell, macrophages play a key role in the inflammatory response. For a long time, the role of pulmonary macrophages in ARDS has tended to revolve around the polarization of M1/M2. However, with the development of single-cell RNA sequencing, fate mapping, metabolomics, and other new technologies, a deeper understanding of the development process, classification, and function of macrophages in the lung are acquired. Here, we discuss the function of pulmonary macrophages in ARDS from the two dimensions of anatomical location and cell origin and describe the effects of cell metabolism and intercellular interaction on the function of macrophages. Besides, we explore the treatments for targeting macrophages, such as enhancing macrophage phagocytosis, regulating macrophage recruitment, and macrophage death. Considering the differences in responsiveness of different research groups to these treatments and the tremendous dynamic changes in the gene expression of monocyte/macrophage, we discussed the possibility of characterizing the gene expression of monocyte/macrophage as the biomarkers. We hope that this review will provide new insight into pulmonary macrophage function and therapeutic targets of ARDS.

Lipocalin-2 promotes acute lung inflammation and oxidative stress by enhancing macrophage iron accumulation

“…International Publisher activated macrophage M1 phenotype or into alternatively M2 phenotype in the presence of interleukin (IL)-4 and IL-13 [4,5]. In particular, the elevation of M1-like genes using genome-wide transcriptional profiling is associated with death on the first day in alveolar macrophages of the BALF taken from patients with ARDS [6,7]. Although activated macrophages play a role in inflammation and phagocytosis in response to acute lung damage, the molecular mechanisms responsible for engaging activated macrophages are still poorly understood.…”

Bioengineered Neutrophil Extinguisher Targets Cascade Immune Pathways of Macrophages for Alleviating Cytokine Storm in Pneumonia

“…45 We therefore performed CD45 immunohistochemical staining and flow cytometry to identify leukocytes in lung tissues after the treatments. Figure 7h and Figures S19 and S20 show that Extinguisher lowered the population of CD45 + cells in the lung tissues, compared with NEs@Lip@M and NEs@Lip@H. In addition, since CD11b lo F4/80 hi resident macrophages play a crucial role in acute respiratory distress syndrome/acute lung injury (ARDS/ALI), 46 we next measured macrophages in lung tissues. In the acute phase of inflammation, resident macrophages reprogram toward the classically activated phenotype (M1) and release various proinflammatory factors.…”

The role of immunometabolism in macrophage polarization and its impact on acute lung injury/acute respiratory distress syndrome

“…IMs are located in the parenchyma between the microvascular endothelium and alveolar epithelium and comprise 30%-40% of lung macrophages ( 22 , 31 ). IMs are initially derived from yolk sac macrophages and fetal liver monocytes and then replenished by circulating progenitor cells for their maintenance in adults ( 22 , 32 ). IMs are involved in tissue remodeling and maintenance of lung homeostasis and antigen presentation as well as affect dendritic cell function to prevent airway allergy ( 33 – 35 ).…”