Inhibiting the Nrf2/HO-1 signaling cascade weakens the pro-inflammatory response induced by gasoline engine exhaust in lung epithelial cells following air-liquid interface exposure

Key Points

• The aim is to evaluate the role of Nrf2/HO-1 signaling in regulating lung inflammation caused by gasoline engine exhaust.
• In vitro exposure of lung epithelial cells to gasoline engine exhaust at air-liquid interface.
• Inhibition of Nrf2/HO-1 signaling to assess effects on inflammation.
• Nrf2/HO-1 inhibition led to a significant reduction in pro-inflammatory response.
• Findings suggest that Nrf2/HO-1 pathway is a crucial regulator in GEE-induced pulmonary inflammation.