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Fig. 6 | Particle and Fibre Toxicology

Fig. 6

From: Role of different mechanisms in pro-inflammatory responses triggered by traffic-derived particulate matter in human bronchiolar epithelial cells

Fig. 6

Comparison of road tunnel PM to particles from stone materials in the pavement and to DEP, and the role of AhR and ROS, in gene expression of IL-1α, CXCL8 and COX2 in HBEC3-KT cells. The cells were exposed to 100 µg/mL (10.4 µg/cm2) coarse (C), fine (F) and ultrafine (UF) PM sampled in the Marienborg and Hell tunnels and to particles derived from the stone materials rhomb porphyry (RP) and quartz diorite (QD) (100 µg/mL (10.4 µg/cm2)) (b, c, f, g, j, k). The cells were also exposed to 100 µg/mL (10.4 µg/cm2) DEP in separate experiments (d, h, l). To assess the role of AhR and ROS, the cells were treated with the AhR-inhibitor CH223191 (1 µM) and the anti-oxidant N-acetyl cysteine (NAC, 5 mM) 1 h before and during particle exposure. Gene expression of IL-1α (a, b, c, d), CXCL8 (e, f, g, h) and COX2 (i, j, k, l) was measured after 6 or 20 h exposure by qPCR. The data are presented as the mean ± SEM of 4–5 independent experiments. *Significant different compared to control. Brackets, significant less responses of stone materials compared to the different sizes of road tunnel PM. # Significant reduction compared to cells without inhibitor. The statistical analysis was performed by two-Way ANOVA with Dunnett’s multiple comparison test

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