Ubiquitous environmental contaminants such as dioxins have long been implicated in cellular toxicity, but only recently have various biological effects been linked to immune regulation. These plentiful noxious agents exert their effects through the arylhydrocarbon receptor (AhR) recognized as a ligand-activated transcription factor. AhR activation mediates gene alteration, cell-cell adhesion interaction, cytokine expression, and mucin production, which are involved in the induction of cancer or inflammation. We have reported that human bronchial epithelial cells express AhR, and AhR activation induces mucin production through reactive oxygen species. This review discusses the role of AhR in lung disease, focusing in particular on airway epithelial cells. In addition, although it is not yet clear how the activation of AhR modifies carcinogenesis or airway inflammation, we mention a potent therapeutic target for AhR activation in the prevention/treatment of lung cancer, allergic asthma, and chronic obstructive pulmonary disease.
All Science Journal Classification (ASJC) codes
- Immunology and Allergy