Extracellular vesicles and endothelial dysfunction in infectious diseases.

Cardiovascular diseases (CVDs) remain the leading cause of mortality and morbidity globally. Studies have shown that infections especially bacteraemia and sepsis are associated with increased risks for endothelial dysfunction and related CVDs including atherosclerosis. Extracellular vesicles (EVs) are small, sealed membrane-derived structures that are released into body fluids and blood from cells and/or microbes and are critically involved in a variety of important cell functions and disease development, including intercellular communications, immune responses and inflammation. It is known that EVs-mediated mechanism(s) is important in the development of endothelial dysfunction in infections with a diverse spectrum of microorganisms including , , SARS-CoV-2 (the virus for COVID-19) and . infection is one of the most common infections globally. During infection, EVs can carry components, such as lipopolysaccharide, cytotoxin-associated gene A, or vacuolating cytotoxin A, and transfer these substances into endothelial cells, triggering inflammatory responses and endothelial dysfunction. This review is to illustrate the important role of EVs in the pathogenesis of infectious diseases, and the development of endothelial dysfunction in infectious diseases especially infection, and to discuss the potential mechanisms and clinical implications.