TLR4 and asthma: EVs not only serve as functional delivery vehicles for TN-C but also significantly potentiate the secretion of key inflammatory mediators including IL-8, IL-6, and CCL5 by macrophages and airway epithelial cells through Toll-like receptor 4 (TLR4)-independent signaling pathways, thereby playing a central pro-inflammatory role in viral-induced asthma exacerbations.