TLR4 and infection: Recent environmental epidemiology reveals that air pollutants can breach traditional infection control barriers: PM2.5 transports endotoxins across alveolar barriers, activating systemic inflammation via Toll-like receptor 4 (TLR4) and impairing fibroblast migration/angiogenesis; NO2 triggers excessive neutrophil extracellular trap (NET) release, creating DNA scaffolds for bacterial biofilm formation; and while ozone (O3) has broad-spectrum antimicrobial properties, chronic exposure depletes surfactant protein A (SP-A), compromising macrophage clearance of Staphylococcus aureus.