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Ascorbic acid enhances the redox cycle between Fe 3+ and Fe 2+ (Fe 3+ Fe 2+ ) as a catalyst in the Fenton reaction, increasing the degree of damage to hydroxyl radicals (Timoshnikov et al

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BMC Microbiol 12 , 18 (2012)

however, in multiple macrophage research models, it is associated with IL-10 upregulation, suppression of pro-inflammatory signaling, and tolerance-related phenotypes ( In addition to host enzymatic systems, the gut microbiota can also convert Trp into a variety of indole derivatives, such as indole-3-acetic acid, and these metabolites can likewise act as AhR ligands to participate in the regulation of mucosal immune homeostasis and may alter inflammatory outcomes by affecting the immunoregulatory programs of local macrophages/mononuclear phagocytes ( Overall, Trp metabolism influences the functional spectrum of macrophages through two intertwined pathways, namely the stress response induced by Trp depletion and the AhR signaling mediated by Kyn/indole derivatives. The overall outcome is often manifested as restriction of pro-inflammatory programs and support of immunoregulatory/tolerance-related phenotypes, although this effect is condition-dependent and influenced by ligand source (host or microbial), inflammatory stage, and the tissue microenvironment