Serum-derived exosomes from house dust mite-sensitized guinea pigs contribute to inflammation in BEAS-2B cells via the TLR4-NF-κB pathway

Airway epithelial cells, which are the first physical defense barrier against allergens, play a pivotal role in immunity, airway inflammation and airway remodeling. The damage and dysfunction of these cells trigger the development of airway inflammatory diseases. Exosomes, which exist in various bodily fluids, mediate cell-cell communication and participate in the immune response process. The present study aimed to investigate whether serum exosomes play a pro-inflammatory role in bronchial epithelial cells (BEAS-2B cells) and, if so, explore the underlying molecular mechanisms. A guinea pig model of House dust mite (HDM)-induced asthma was established by sensitizing the rodents with HDM and PBS, and serum-derived exosomes were harvested. It was found that serum-derived exosomes from HDM-sensitized guinea pigs displayed higher levels of exosomal markers than those from controls. Additionally, western blot analysis and reverse transcription-quantitative PCR indicated that serum-derived exosomes from HDM-sensitized guinea pigs carried heat shock protein 70 and triggered an inflammatory response in BEAS-2B cells via the toll-like receptor 4 (TLR4)-NF-κB pathway. However, TAK-242, an inhibitor of the expression of TLR4, blocked the activation of the TLR4-NF-κB pathway. These findings provided a novel mechanism for exosome-mediated inflammatory responses and a new perspective for the intervention of inflammatory airway disorders.