Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

• Published in: Journal of toxicology and environmental health. Part B, Critical reviews Vol. 21; no. 3; pp. 142 - 160
• Main Authors: Benedikter, Birke J., Wouters, Emiel F. M., Savelkoul, Paul H. M., Rohde, Gernot G. U., Stassen, Frank R. M.
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 01-01-2018; Taylor & Francis Ltd
• Subjects: Air pollution; Air Pollution - adverse effects; Angiogenesis; Asthma; Biomarkers; Blood plasma; Cardiovascular diseases; Cellular stress response; Chronic Disease; Chronic illnesses; Chronic obstructive pulmonary disease; Cigarette smoke; Etiology; Exosomes; Exposure; Extracellular vesicles; Extracellular Vesicles - drug effects; Flow cytometry; Health risks; Heart diseases; Humans; Lung cancer; Lung diseases; Microparticles; Obstructive lung disease; Particulate matter; Pollution; Respiratory Tract Diseases - chemically induced; Scientific papers; Search engines; Smoke; Stresses; Thromboembolism; Thrombosis; Tobacco; Vesicles
• ISSN: 1093-7404; 1521-6950
• DOI: 10.1080/10937404.2018.1466380

Extracellular vesicles (EV) are secreted signaling entities that enhance various pathological processes when released in response to cellular stresses. Respiratory exposures such as cigarette smoke and air pollution exert cellular stresses and are associated with an increased risk of several chronic diseases. The aim of this review was to examine the evidence that modifications in EV contribute to respiratory exposure-associated diseases. Publications were searched using PubMed and Google Scholar with the search terms (cigarette smoke OR tobacco smoke OR air pollution OR particulate matter) AND (extracellular vesicles OR exosomes OR microvesicles OR microparticles OR ectosomes). All original research articles were included and reviewed. Fifty articles were identified, most of which investigated the effect of respiratory exposures on EV release in vitro (25) and/or on circulating EV in human plasma (24). The majority of studies based their main observations on the relatively insensitive scatter-based flow cytometry of EV (29). EV induced by respiratory exposures were found to modulate inflammation (19), thrombosis (13), endothelial dysfunction (11), tissue remodeling (6), and angiogenesis (3). By influencing these processes, EV may play a key role in the development of cardiovascular diseases and chronic obstructive pulmonary disease and possibly lung cancer and allergic asthma. The current findings warrant additional research with improved methodologies to evaluate the contribution of respiratory exposure-induced EV to disease etiology, as well as their potential as biomarkers of exposure or risk and as novel targets for preventive or therapeutic strategies.