Background: Around one-third of Australians reported having chronic respiratory conditions. Extracellular vesicles (EV) are secreted signalling entities that enhance various pathological processes when released in response to cellular stresses, which are regarded as essential messengers in intercellular communication. The study aims to explore the role of EVs in the development and/or progression of PM2.5-induced chronic inflammatory lung diseases.

Method: EVs were collected from epithelium cells under the stimulation of PM2.5. Human fibroblast cells can uptake and be activated by EVs, producing an extracellular matrix. RNA-Seq will be used to explore the differences of the component inside EV induced by PM2.5 followed by Crisper-cas9.

Results: The expression of fibronectin, collagen 4, and ?SMA increased in human fibroblast cells. EVs triggered the inflammatory response in fibroblast cells. However, the component of EVs is still unclear now.

Conclusion: PM2.5 can improve epithelial regulation of fibroblasts to myofibroblasts transition, leading to subepithelial fibrosis and extracellular matrix deposition. EVs secreted from epithelium cells stimulated by PM2.5 could modulate the biological functions of fibroblast cells. However, the current findings warrant additional research to evaluate the contribution of respiratory exposure-induced EV to disease aetiology, and as novel targets for preventive or therapeutic strategies.