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자료유형
학술저널
저자정보
Fei Hou (Chinese PLA General Hospital) Huan Wang (Beijing Institute of Lifeomics) Kun Zheng (Beijing Institute of Lifeomics) Wenting Yang (Beijing Institute of Lifeomics) Kun Xiao (Chinese PLA General Hospital) Zihan Rong (Hebei University) Junjie Xiao (Chinese PLA General Hospital) Jing Li (Beijing Institute of Lifeomics) Baihe Cheng (Beijing Institute of Lifeomics) Li Tang (Beijing Institute of Lifeomics) Lixin Xie (Chinese PLA General Hospital)
저널정보
대한면역학회 Immune Network Immune Network Vol.23 No.3
발행연도
2023.6
수록면
33 - 48 (16page)

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In acute lung injury, two subsets of lung macrophages exist in the alveoli: tissue-resident alveolar macrophages (AMs) and monocyte-derived alveolar macrophages (MDMs). However, it is unclear whether these 2 subsets of macrophages have different functions and characteristics during the recovery phase. RNA-sequencing of AMs and MDMs from the recovery period of LPS-induced lung injury mice revealed their differences in proliferation, cell death, phagocytosis, inflammation and tissue repair. Using flow cytometry, we found that AMs showed a higher ability to proliferate, whereas MDMs expressed a larger amount of cell death. We also compared the ability of phagocytosing apoptotic cells and activating adaptive immunity and found that AMs have a stronger ability to phagocytose, while MDMs are the cells that activate lymphocytes during the resolving phase. By testing surface markers, we found that MDMs were more prone to the M1 phenotype, but expressed a higher level of pro-repairing genes. Finally, analysis of a publicly available set of single-cell RNA-sequencing data on bronchoalveolar lavage cells from patients with SARS-CoV-2 infection validated the double-sided role of MDMs. Blockade of inflammatory MDM recruitment using CCR2−/− mice effectively attenuates lung injury. Therefore, AMs and MDMs exhibited large differences during recovery. AMs are long-lived M2-like tissue-resident macrophages that have a strong ability to proliferate and phagocytose. MDMs are a paradoxical group of macrophages that promote the repair of tissue damage despite being strongly pro-inflammatory early in infection, and they may undergo cell death as inflammation fades. Preventing the massive recruitment of inflammatory MDMs or promoting their transition to pro-repairing phenotype may be a new direction for the treatment of acute lung injury.

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ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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