Fig. 11.

Mechanism for dust extract induction of inflammatory gene expression. Treatment of lung epithelial cells with dust extracts increases intracellular reactive oxygen species (ROS) levels causing oxidative stress and leading to STAT-3 activation mediated by nonreceptor tyrosine-protein kinase 2 (TYK2) and epidermal growth factor receptor (EGFR) tyrosine kinases. Activated STAT-3 is translocated to the nucleus, where it binds to cognate promoter DNA elements to increase transcription of immune and inflammatory genes. The effects of ROS induced by dust extract on activation of TYK2 and EGFR are not known. The “P” inside an oval represents phosphorylation.