Extracellular vesicles in obesity and its associated inflammation

Abstract

Obesity is characterized by low-grade, chronic inflammation, which promotes insulin resistance and diabetes. Obesity can lead to the development and progression of many autoimmune diseases, including inflammatory bowel disease, psoriasis, psoriatic arthritis, rheumatoid arthritis, thyroid autoimmunity, and type 1 diabetes mellitus (T1DM). These diseases result from an alteration of self-tolerance by promoting pro-inflammatory immune response by lowering numbers of regulatory T cells (T_regs), increasing Th1 and Th17 immune responses, and inflammatory cytokine production. Therefore, understanding the immunological changes that lead to this low-grade inflammatory milieu becomes crucial for the development of therapies that suppress the risk of autoimmune diseases and other immunological conditions. Cells generate extracellular vesicles (EVs) to eliminate cellular waste as well as communicating the adjacent and distant cells through exchanging the components (genetic material [DNA or RNA], lipids, and proteins) between them. Immune cells and adipocytes from individuals with obesity and a high basal metabolic index (BMI) produce also release exosomes (EXOs) and microvesicles (MVs), which are collectively called EVs. These EVs play a crucial role in the development of autoimmune diseases. The current review discusses the immunological dysregulation that leads to inflammation, inflammatory diseases associated with obesity, and the role played by EXOs and MVs in the induction and progression of this devastating conditi8on.

GRAPHICAL ABSTRACT

Conflict of interest statement

The authors declare not having any competing interests that might influence this study or no involvement of study sponsors.

Authors’ contributions

V.K. conceived the idea and wrote the manuscript. U.S. edited the manuscript. S. Kumar edited the manuscript. S.K. made the figures and assisted V.K. in the writing of the manuscript.

Acknowledgment

The authors thank the UTHSC Office of Scientific Writing for the critical review of the manuscript.

Additional information

Funding

This study was supported in part by grants from NIAID R01 AI140405 (UPS) at UTHSC, Memphis.