Reactive oxygen species generation pathways in mucosal and inflammatory cells (ROS generation pathways)

Reactive oxygen species (ROS) generation pathways in mucosal and inflammatory cells represent a complex network of enzymatic and non-enzymatic processes that produce highly reactive oxygen-containing molecules. The primary enzymatic sources include the NADPH oxidase (NOX) family, particularly NOX2 in phagocytes and NOX1/DUOX2 in mucosal epithelial cells, as well as mitochondrial electron transport chain leakage and myeloperoxidase (MPO) activity [1][2]. While ROS are essential for host defense and intracellular signaling at physiological levels, their overproduction leads to oxidative stress, which is a hallmark of chronic inflammatory diseases such as ulcerative colitis and Crohn's disease [3]. In these conditions, excessive ROS cause direct damage to cellular components like lipids and DNA, while also activating pro-inflammatory transcription factors like NF-κB [2]. Pharmacological intervention typically involves the use of antioxidants, ROS scavengers like Sulfasalazine, or specific inhibitors of NOX enzymes to mitigate tissue damage [4]. However, targeting these pathways is challenging because ROS are also required for normal immune function and wound healing, meaning non-specific inhibition can lead to immunosuppression or impaired mucosal repair [1][5]. [1] Lambeth, J. D. (2004). Nature Reviews Immunology. [2] Mittal, M., et al. (2014). Antioxidants & Redox Signaling. [3] Aviello, G., & Knaus, U. G. (2017). British Journal of Pharmacology. [4] Piechota-Polanczyk, A., & Fichna, J. (2014). Alimentary Pharmacology & Therapeutics. [5] Vermot, A., et al. (2021). Antioxidants.

Other names

ROS production pathwaysOxidative stress generationPhagocyte respiratory burstMucosal oxidative pathwaysRedox signaling pathways

Inhibition of NADPH oxidase enzymes (NOX1, NOX2, DUOX2), scavenging of reactive oxygen species, and modulation of mitochondrial electron transport chain activity.