Iron overload and tuberculosis: a case for iron chelation therapy.
Elevated levels of iron impair immune defence mechanisms, and specifically the macrophage function of innate immunity. Iron enhances Mycobacterium tuberculosis infection, M. tuberculosis replication, progression to clinical disease and death from tuberculosis (TB). Chelation of iron in individuals with an excessive iron burden may reduce M. tuberculosis viability and replication, restore host defence mechanisms and could find application in the prevention and treatment strategies in settings where both iron overload and TB are prevalent. The objective of this paper was to summarise recent literature on the role of iron in TB pathogenesis and to examine the potential of iron chelation therapy. The literature confirms a key role for iron in mycobacterial virulence. The ability of chelation to enhance host effector mechanisms and to inhibit replication of various pathogens justifies further studies into iron chelation as a potential additive therapy for TB.
Cronje
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L
Division of Biochemistry, Department of Chemistry and Biochemistry, University of Johannesburg, Auckland Park, South Africa.
Bornman
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L
D002614:Chelating Agents / Q000627:therapeutic use*; D018450:Disease Progression; D006801:Humans; D019190:Iron Overload / Q000150:complications* / Q000188:drug therapy*; D009169:Mycobacterium tuberculosis / Q000472:pathogenicity; D014397:Tuberculosis, Pulmonary / Q000150:complications*; D014774:Virulence
D002614:Chelating Agents