Macrophage function in adipose tissue homeostasis and metabolic inflammation

The adipose tissue is rich in immune cells. In this Review, the authors cover adipose tissue myeloid cells and how they control and respond to inflammation and pathology. Obesity-related metabolic organ inflammation contributes to cardiometabolic disorders. In obese individuals, changes in lipid fluxes and storage elicit immune responses in the adipose tissue (AT), including expansion of immune cell populations and qualitative changes in the function of these cells. Although traditional models of metabolic inflammation posit that these immune responses disturb metabolic organ function, studies now suggest that immune cells, especially AT macrophages (ATMs), also have important adaptive functions in lipid homeostasis in states in which the metabolic function of adipocytes is taxed. Adverse consequences of AT metabolic inflammation might result from failure to maintain local lipid homeostasis and long-term effects on immune cells beyond the AT. Here we review the complex function of ATMs in AT homeostasis and metabolic inflammation. Additionally, we hypothesize that trained immunity, which involves long-term functional adaptations of myeloid cells and their bone marrow progenitors, can provide a model by which metabolic perturbations trigger chronic systemic inflammation.

Automated summary

This review focuses on adipose tissue myeloid cells and their role in controlling and responding to inflammation and pathology. Obesity-related metabolic organ inflammation is a contributing factor to cardiometabolic disorders. Immune responses in adipose tissue, including expansion of immune cell populations and changes in their function, are triggered by alterations in lipid fluxes and storage in obese individuals. Recent studies suggest that adipose tissue macrophages (ATMs), a type of immune cell, also play important roles in lipid homeostasis. The review discusses the complex function of ATMs in adipose tissue homeostasis and metabolic inflammation. It also proposes that trained immunity, which involves long-term functional adaptations of myeloid cells, may be responsible for chronic systemic inflammation triggered by metabolic perturbations.