Mechanistic profiling of oxidative stress, cytokine responses, and NF-κB/TLR4 signaling induced by biomass-derived particulate organic extracts in a human lung epithelial-macrophage co-culture model.

induces source-dependent oxidative and inflammatory responses and identify epithelial-macrophage crosstalk as an important mechanism amplifying inflammatory signaling. The results also support the value of co-culture models for mechanistic hazard identification of biomass-burning emissions.