Figure 5From: Polycyclic aromatic hydrocarbon components contribute to the mitochondria-antiapoptotic effect of fine particulate matter on human bronchial epithelial cells via the aryl hydrocarbon receptorThe antiapoptotic effect is not correlated with proinflammatory cytokines release after PM 2.5 exposure. (A) Proinflammatory potential of different batches of PM2.5 10 μg/cm2 (AW, AS, VW and VS) on 16HBE cells. After 4 h or 24 h particle exposure, Amphiregulin (AR) and granulocyte monocyte colony-stimulating factor (GM-CSF) secretion were evaluated by ELISA. Data are represented as mean ± SD of triplicates. * indicates significance at p < 0.001, treated vs. control. (B) Flow cytometric analysis was done as before in the presence or absence of PM2.5-AW pretreatement and/or apoptosis inducer A23187 (3 μM). The implication of the EGFR was evaluated using the recombinant EGF ligand (rEGF 150 ng/ml) or the inhibitor AG1478 (1 μM). Data are represented as mean ± SD of three independent results (* treated vs. control p < 0.05; # vs. A23187 alone, p < 0.05).Back to article page