Metabolic adaption of epithelial cells in asthma: a window to the initiation of carcinogenesis?

Abstract

Recent data has resulted in an interest in the metabolic shift in cellular metabolism to aerobic glycolysis, increased reactive oxygen species (ROS), and mitochondrial dysfunction associated with asthma. There has been a push to better understand the immune and metabolic changes in allergy to improve understanding of disease pathology and treatment. Aerobic glycolysis seen in epithelial cells in asthma promotes chronic inflammation and the production of inflammatory cytokines. Asthma epithelial cells share a number of features proposed in the stages of cancer initiation including aerobic glycolysis and increased apoptosis with proliferation, all within a chronic inflammatory microenvironment. Metabolic reprogramming in malignant cells has been widely investigated since the glycolytic characteristics were first described last century. It is still debated whether these metabolic changes are the cause or consequence of carcinogenesis and oncogenic cell-selective pressures. Although historic results have been conflicting, recent data has found an increased lung cancer risk in asthma patients, independent of risk factors. A review of emerging research on the metabolic changes seen in asthma helps us to propose a pathway between the initiation of aerobic glycolysis and the selective pressures of the epithelial microenvironment and resulting malignant transformation risk.