Etiology of lipid-laden macrophages in the lung

TY - JOUR

T1 - Etiology of lipid-laden macrophages in the lung

AU - Stevenson, E. R.

AU - Smith, L. C.

AU - Wilkinson, M. L.

AU - Lee, S. J.

AU - Gow, A. J.

N1 - Funding Information: This work was supported by the National Heart, Lung, and Blood Institute [Grant HL086621]; and the National Institute of Environmental Health Sciences [Grant T32ES01984; P30ES005022], ES030984, ES032473. Publisher Copyright: © 2023 Elsevier B.V.

PY - 2023/10

Y1 - 2023/10

N2 - Uniquely positioned as sentinel cells constantly exposed to the environment, pulmonary macrophages are vital for the maintenance of the lung lining. These cells are responsible for the clearance of xenobiotics, pathogen detection and clearance, and homeostatic functions such as surfactant recycling. Among the spectrum of phenotypes that may be expressed by macrophages in the lung, the pulmonary lipid-laden phenotype is less commonly studied in comparison to its circulatory counterpart, the atherosclerotic lesion-associated foam cell, or the acutely activated inflammatory macrophage. Herein, we propose that lipid-laden macrophage formation in the lung is governed by lipid acquisition, storage, metabolism, and export processes. The cellular balance of these four processes is critical to the maintenance of homeostasis and the prevention of aberrant signaling that may contribute to lung pathologies. This review aims to examine mechanisms and signaling pathways that are involved in lipid-laden macrophage formation and the potential consequences of this phenotype in the lung.

AB - Uniquely positioned as sentinel cells constantly exposed to the environment, pulmonary macrophages are vital for the maintenance of the lung lining. These cells are responsible for the clearance of xenobiotics, pathogen detection and clearance, and homeostatic functions such as surfactant recycling. Among the spectrum of phenotypes that may be expressed by macrophages in the lung, the pulmonary lipid-laden phenotype is less commonly studied in comparison to its circulatory counterpart, the atherosclerotic lesion-associated foam cell, or the acutely activated inflammatory macrophage. Herein, we propose that lipid-laden macrophage formation in the lung is governed by lipid acquisition, storage, metabolism, and export processes. The cellular balance of these four processes is critical to the maintenance of homeostasis and the prevention of aberrant signaling that may contribute to lung pathologies. This review aims to examine mechanisms and signaling pathways that are involved in lipid-laden macrophage formation and the potential consequences of this phenotype in the lung.

KW - Foam cell

KW - Immunometabolism

KW - Inflammation

KW - Lipid

KW - Lung

KW - Macrophage

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U2 - https://doi.org/10.1016/j.intimp.2023.110719

DO - https://doi.org/10.1016/j.intimp.2023.110719

M3 - Review article

C2 - 37595492

SN - 1567-5769

VL - 123

JO - International Immunopharmacology

JF - International Immunopharmacology

M1 - 110719

ER -