Publications

Tuberculosis (TB) unfolds within a chemically reactive battlefield where host-derived reactive oxygen and nitrogen species (ROS/RNS) intersect with immune signaling to shape disease outcomes. While oxidative stress is essential for mycobacterial control, sustained redox imbalance damages host tissues, disrupts granuloma integrity, fuels inflammation, and may even enhance Mycobacterium tuberculosis (Mtb) persistence. This review synthesizes current understanding of redox–immune crosstalk in TB pathogenesis and critically evaluates antioxidant phytochemicals as host-directed therapy (HDT) candidates. We outline how key pathways-Nrf2/Keap1, NF-κB, HIF-1α, MAPK, and JAK/STAT-integrate redox signals to calibrate macrophage activation, autophagy, antigen presentation, and adaptive immunity. We then survey major phytochemical classes (polyphenols, terpenoids, organosulfur compounds, alkaloids) with reported effects on ROS/RNS homeostasis, inflammasome activity, mitochondrial function, and immunometabolism. Emerging data suggest that select compounds can (i) enhance bactericidal mechanisms without exacerbating tissue injury, (ii) temper pathological inflammation, (iii) promote autophagy and phagosome maturation, and (iv) mitigate anti-TB drug toxicities. We highlight formulation advances that improve bioavailability, summarize preclinical/early clinical signals, and discuss safety, pharmacokinetic, and drug–drug interaction considerations. Finally, we identify knowledge gaps and propose a translational roadmap for integrating rigorously characterized phytochemicals into TB HDT regimens.