The critical role of iron in some clinical infections

Bullen, J. J.; Ward, C. Gillon; Rogers, H. J.

doi:10.1007/bf01975810

Cited by 72 publications

(31 citation statements)

References 38 publications

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“…36 Iron may contribute to HCV-related liver disease by facilitating viral replication, possibly by provision of nutrients to the virus as has been suggested for hepatitis B virus 37 and other viruses and bacteria. 38,39 Iron is an essential cofactor for RNA replication. A number of factors are, however, against this theory.…”

Section: Discussionmentioning

confidence: 99%

Heterozygosity for hereditary hemochromatosis is associated with more fibrosis in chronic hepatitis C

et al. 1998

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Hepatic iron has been associated with more aggressive liver disease in chronic viral hepatitis. We evaluated whether the recently described C282Y mutation of the hemochromatosis gene, designated HFE (responsible for at least 83% of hereditary hemochromatosis), was associated with more advanced liver disease in chronic hepatitis C. One hundred thirty-seven patients with biopsy-proven chronic hepatitis C were studied and liver biopsies scored for necroinflammation (grade 0-18) and fibrosis (stage 0-6). Genomic DNA was amplified by polymerase chain reaction and the C282Y mutation identified by restriction with RsaI and electrophoretic separation of restriction fragments. Ten (7.3%) patients had the C282Y mutation. No C282Y homozygous patients were identified. Age, sex distribution, and estimated weekly alcohol consumption were not significantly different between those with and without the mutation. Serum ferritin was higher in the heterozygotes (mean, 339 g/L) compared with homozygous wild types (153 g/L; P ‫؍‬ .0005). In the majority of patients, liver iron was graded 0 out of 4, but hepatocyte iron staining was more commonly present in heterozygotes compared with homozygous normals (30% compared with 4% [P ‫؍‬ .02]). Liver disease was more advanced in those with the mutant allele (mean fibrosis stage: 3.6, compared with wild type: 1.5 [P ‫؍‬ .01]). Cirrhosis was found more often in those with the mutation (40%) compared with those without (8.7%) (P ‫؍‬ .01; odds ratio: 7.6 [1.9-31.2]). There was no significant difference in inflammation scores between heterozygotes and wild type (mean, 5.4 compared with 4

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Section: Discussionmentioning

confidence: 99%

Heterozygosity for hereditary hemochromatosis is associated with more fibrosis in chronic hepatitis C

et al. 1998

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“…Nonlethal injections of E. coli in guinea pigs become lethal by the concomitant addition of either heme or enough iron to saturate the transferrin (9,20). The virulence of Yersinia enterocolitica is enhanced 10 million-fold by the peritoneal injection of ferric desferrioxamine (17,21). A similar effect is seen if desferrioxamine is supplied during infections of Klebsiella and Salmonella (15), whereas direct correlation between the LD 50 of Vibrio vulnificans and iron availability has been demonstrated (22).…”

Section: Iron: Can't Live With It Can't Live Without Itmentioning

confidence: 94%

Enterobactin: An archetype for microbial iron transport

Raymond

Dertz

Kim

2003

Proc. Natl. Acad. Sci. U.S.A.

809

692

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Bacteria have aggressive acquisition processes for iron, an essential nutrient. Siderophores are small iron chelators that facilitate cellular iron transport. The siderophore enterobactin is a triscatechol derivative of a cyclic triserine lactone. Studies of the chemistry, regulation, synthesis, recognition, and transport of enterobactin make it perhaps the best understood of the siderophore-mediated iron uptake systems, displaying a lot of function packed into this small molecule. However, recent surprises include the isolation of corynebactin, a closely related trithreonine triscatechol derivative lactone first found in Gram-positive bacteria, and the crystal structure of a ferric enterobactin complex of a protein identified as an antibacterial component of the human innate immune system.

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“…25 Plasma itself demonstrates antimicrobial properties that are attenuated by the addition of iron, whereas inhibition of bacterial growth occurs in iron-deficient conditions. [25][26][27] Hypoferremia is therefore thought to be an innate antimicrobial strategy. This may explain the increased rates of infection seen among patients with β-thalassemia major who have iron overload.…”

Section: Anemia As An Adaptive Physiologic Responsementioning

confidence: 99%