Mesenchymal stem cells influence monocyte/macrophage phenotype: Regulatory mode and potential clinical applications.

Mesenchymal stem cells (MSCs) are pluripotent stem cells derived from a variety of tissues, such as umbilical cord, fat, and bone marrow. Today, MSCs are widely recognized for their prominent anti-inflammatory properties in a variety of acute and chronic inflammatory diseases. In inflammatory diseases, monocytes/macrophages are an important part of the innate immune response in the body, and the alteration of the inflammatory phenotype plays a crucial role in the secretion of pro-inflammatory/anti-inflammatory factors, the repair of injured sites, and the infiltration of inflammatory cells. In this review, starting from the effect of MSCs on the monocyte/macrophage phenotype, we have outlined in detail the process by which MSCs influence the transformation of the monocyte/macrophage inflammatory phenotype, emphasizing the central role of monocytes/macrophages in MSC-mediated anti-inflammatory and damage site repair. MSCs are phagocytosed by monocytes/macrophages in various physiological states, the paracrine effect of MSCs and mitochondrial transfer of MSCs to macrophages to promote the transformation of monocytes/macrophages into anti-inflammatory phenotypes. We also review the clinical applications of the MSCs-monocytes/macrophages system and describe novel pathways between MSCs and tissue repair, the effects of MSCs on the adaptive immune system, and the effects of energy metabolism levels on monocyte/macrophage phenotypic changes. [Display omitted] • Mesenchymal stem cells convert monocytes/macrophages to an anti-inflammatory phenotype in three main ways. • Mesenchymal stem cells contribute to monocyte/macrophage phenotypic transformation through phagocytosis by monocytes/macrophages. • Paracrine actions of mesenchymal stem cells can induce monocytes/macrophages to switch to an anti-inflammatory phenotype. • Mitochondrial transfer from mesenchymal stem cells to macrophages can promote their conversion to an anti-inflammatory phenotype. [ABSTRACT FROM AUTHOR]