Etiology of lipid-laden macrophages in the lung

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.

Automated summary

Pulmonary macrophages, as sentinel cells exposed to the environment, play a vital role in maintaining lung health. The formation of lipid-laden macrophages in the lungs is governed by lipid acquisition, storage, metabolism, and export processes. Understanding the mechanisms and signaling pathways involved in this process is essential for maintaining homeostasis and preventing lung pathologies.