Allergic inflammatory diseases, such as asthma and allergic rhinitis, are caused by a complex interaction between genetic and environmental factors. Although several relevant candidate genes that are associated with environmental pollutants and allergic diseases have been identified in previous studies, the mechanisms underlying the induction of cytokines and chemokines by environmental pollutants and their role in human diseases are still unclear. This study examines the correlation between exposure to toluene, which is a common environmental pollutant, and the expression of immune-related genes, using reverse transcription-polymerase chain reaction (RT-PCR) with pathway-targeted arrays (RT2 Profiler™ PCR Arrays). Our PCR array analyses suggested the p38 MAPK and JNK pathways are activated upon toluene treatment in BEAS-2B cells, based on the expression profiles of MAPK8 (JNK1), MAPK9 (JNK2), MAPK10 (JNK3), MAPK11 (P38BETA2), CCL5 (RAN TES), CCL11 (eotaxin), and genes encoding proinflammatory cytokines, including tumor necrosis factor (TNF), TOLLIP, IL1A, and IL1B. This study aims to show that toluene exposure induces the expression of RANTES and eotaxin in cultured human bronchial epithelial cell lines through two distinct MAPKs, p38 and JNK.
- Allergic inflammatory diseases
- Bronchial epithelial cells
- Gene expression profiles
- PCR array
ASJC Scopus subject areas
- Health, Toxicology and Mutagenesis