Journal
INFECTION AND IMMUNITY
Volume 78, Issue 12, Pages 4977-4989Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.00613-10
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Funding
- Southeastern Regional Center of Excellence for Emerging Infections and Biodefense [U54 AI057157-06]
- National Institute of Allergy and Infectious Diseases, NIH [AI069233, AI073843, 5 T32 HL069765]
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Virtually all bacterial pathogens require iron to infect vertebrates. The most abundant source of iron within vertebrates is in the form of heme as a cofactor of hemoproteins. Many bacterial pathogens have elegant systems dedicated to the acquisition of heme from host hemoproteins. Once internalized, heme is either degraded to release free iron or used intact as a cofactor in catalases, cytochromes, and other bacterial hemoproteins. Paradoxically, the high redox potential of heme makes it a liability, as heme is toxic at high concentrations. Although a variety of mechanisms have been proposed to explain heme toxicity, the mechanisms by which heme kills bacteria are not well understood. Nonetheless, bacteria employ various strategies to protect against and eliminate heme toxicity. Factors involved in heme acquisition and detoxification have been found to contribute to virulence, underscoring the physiological relevance of heme stress during pathogenesis. Herein we describe the current understanding of the mechanisms of heme toxicity and how bacterial pathogens overcome the heme paradox during infection.
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