The Role of Macrophages and Alveolar Epithelial Cells in the Development of ARDS

Acute lung injury (ALI) usually causes acute respiratory distress syndrome (ARDS), or even death in critical ill patients. Immune cell infiltration in inflamed lungs is an important hallmark of ARDS. Macrophages are a type of immune cell that participate in the entire pathogenic trajectory of ARDS a...

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Bibliographic Details
Published in:Inflammation 2023-02, Vol.46 (1), p.47-55
Main Authors: Tao, Huan, Xu, Younian, Zhang, Shihai
Format: Article
Language:English
Subjects:
Alveolar Epithelial Cells - metabolism
Alveoli
Anesthesiology
Biomedical and Life Sciences
Biomedicine
Cell death
Coronaviruses
COVID-19
Cytokines
Cytokines - metabolism
Cytology
Epithelial cells
Gene expression
Genotype & phenotype
Homeostasis
Humans
Immune clearance
Immunology
Inflammation
Internal Medicine
Lung - metabolism
Macrophages
Macrophages - metabolism
Macrophages, Alveolar - metabolism
Microorganisms
Neutrophils
Pathogens
Pathology
Permeability
Pharmacology/Toxicology
Pneumonia
Rehabilitation
Respiratory distress syndrome
Respiratory Distress Syndrome - metabolism
Review
Rheumatology
Viral infections
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Summary:Acute lung injury (ALI) usually causes acute respiratory distress syndrome (ARDS), or even death in critical ill patients. Immune cell infiltration in inflamed lungs is an important hallmark of ARDS. Macrophages are a type of immune cell that participate in the entire pathogenic trajectory of ARDS and most prominently via their interactions with lung alveolar epithelial cells (AECs). In the early stage of ARDS, classically activated macrophages secrete pro-inflammatory cytokines to clearance of the pathogens which may damage alveolar AECs cell structure and result in cell death. Paradoxically, in late stage of ARDS, anti-inflammatory cytokines secreted by alternatively activated macrophages dampen the inflammation response and promote epithelial regeneration and alveolar structure remodeling. In this review, we discuss the important role of macrophages and AECs in the progression of ARDS.
ISSN:0360-3997
1573-2576
DOI:10.1007/s10753-022-01726-w