Review demonstrates that reactive oxygen species drive allergic and inflammatory skin diseases, suggesting antioxidant pathways represent viable therapeutic targets.
Key Points
To review the mechanisms by which pro-oxidants, reactive oxygen species, and oxidative stress contribute to the pathogenesis of allergic and inflammatory skin diseases.
Synthesized molecular and cellular evidence regarding pro-oxidant exposure, antioxidant imbalances, and macromolecular damage across common inflammatory skin conditions.
Examined immune signaling cascades, focusing on Toll-like receptor 2 activation in monocytes and FcεRI cross-linking in mast cells.
Imbalances between reactive oxygen species and antioxidant defenses cause oxidative damage to proteins, lipids, and DNA in atopic dermatitis, urticaria, and psoriasis.
Monocytes in atopic dermatitis exhibit heightened reactive oxygen species production in response to the TLR2 ligand zymosan, implicating Staphylococcus aureus colonization in epidermal damage.
FcεRI aggregation on mast cells stimulates intracellular reactive oxygen species generation, which function as downstream secondary messengers to amplify allergic signaling.