IRON DEFICIENCY AND GENETIC REGULATION IN TUBERCULOSIS THROUGH MOLECULAR HOST-PATHOGEN INTERACTIONS

Background: Anemia is a frequent comorbidity in tuberculosis (TB), often driven by chronic inflammation and dysregulated iron metabolism. Elevated hepcidin levels limit iron availability by suppressing ferroportin, leading to functional iron deficiency and impaired erythropoiesis. Objective: This review discusses the molecular mechanisms linking iron metabolism, host immune response, and Mycobacterium tuberculosis persistence, particularly in the context of drug-resistant TB. Content: We summarize current knowledge on the hepcidin–ferroportin axis, siderophore-mediated iron acquisition by M. tuberculosis, and the diagnostic value of biomarkers such as ferritin, transferrin saturation, and soluble transferrin receptor. Considerations for iron therapy, including its risks during active inflammation and emerging targeted treatments, are also addressed. Conclusion: Anemia in TB requires a selective, biomarker-guided approach. While iron supplementation may benefit those with true deficiency, improper use can worsen infection. Targeted modulation of iron pathways offers promising therapeutic alternatives.