Skip to main content
Fig. 5 | Particle and Fibre Toxicology

Fig. 5

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

Fig. 5

Role of AhR and ROS in cytokine release in HBEC3-KT cells after exposure to road tunnel PM particles, stone particles and DEP. The cells were exposed to 100 µg/mL (10.4 µg/cm2) of coarse (C), fine (F) and ultrafine (UF) PM sampled in the Marienborg and Hell tunnels and to 100 µg/mL (10.4 µg/cm2) particles derived from the stone materials rhomb porphyry (RP) and quartz diorite (QD) (a, b, d, e). The cells were also exposed to 100 µg/mL (10.4 µg/cm2) DEP in separate experiments (c, f). 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. Release of IL-1α (a, b, c) and CXCL8 (d, e, f) was determined by ELISA. The data presented represent the mean ± SEM of 4–5 independent experiments. *Significant different from control. #Significant reduction compared to without inhibitor. The statistical analysis was performed by 2-way ANOVA with Dunnett’s comparison test

Back to article page