Extracellular Vesicle/Macrophage Axis: Potential Targets for Inflammatory Disease Intervention

Abstract

Extracellular vesicles (EVs) can regulate the polarization of macrophages in a variety of inflammatory diseases by mediating intercellular signal transduction and affecting the occurrence and development of diseases. After macrophages are regulated by EVs, they mainly show two phenotypes: the proinflammatory M1 type and the anti-inflammatory M2 type. A large number of studies have shown that in diseases such as mastitis, inflammatory bowel disease, Acute lung injury, and idiopathic pulmonary fibrosis, EVs promote the progression of the disease by inducing the M1-like polarization of macrophages. In diseases such as liver injury, asthma, and myocardial infarction, EVs can induce M2-like polarization of macrophages, inhibit the inflammatory response, and reduce the severity of the disease, thus indicating new pathways for treating inflammatory diseases. The EV/macrophage axis has become a potential target for inflammatory disease pathogenesis and comprehensive treatment. This article reviews the structure and function of the EV/macrophage axis and summarizes its biological functions in inflammatory diseases to provide insights for the diagnosis and treatment of inflammatory diseases.

Keywords: M1-like macrophage polarization; M2-like macrophage polarization; extracellular vesicle; inflammation; macrophages.

Figure 1

Particle size, formation process and classification of EVs.

Figure 2

Secretory cells release EVs to induce macrophage polarization through a variety of ways.

Figure 3

The main mechanism of macrophage polarization is in various inflammatory diseases. DCM, dilated cardiomyopathy; AM, acute Mastitis; MIR, myocardial ischemia-reperfusion injury; ALI, Acute lung injury; NAFLD, non-alcoholic fatty liver disease; ORI, Obesity-related inflammation; SI, Skin inflammation; AS, Atherosclerosis; IPF, Idiopathic pulmonary fibrosis; DM, Diabetes mellitus.