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Doe
Sat, Oct-26-02, 13:57
Mass supplementation of iron seems like it may not be such a
good idea .. ?

J Biol Chem 2002 Oct 23;

Intraphagosomal mycobacterium tuberculosis acquires iron from
both extracellular transferrin and intracellular iron pools:
Impact of interferon-gamma and hemochromatosis.

Olakanmi O, Schlesinger LS, Ahmed A, Britigan BE Department of
Internal Medicine, University of Iowa, Iowa City, IA 52242.

[Record supplied by publisher]

Mycobacterium tuberculosis (M.tb) multiplies within the
macrophage phagosome and requires iron (Fe) for growth. We
examined the route(s) by which intracellular M.tb acquires Fe.
During intracellular growth of the virulent Erdman M.tb strain
in human monocyte-derived macrophages (MDM), M.tb acquisition
of 59Fe from transferrin (TF) provided extracellularly
(exogenous source) was compared to acquisition when MDM were
loaded with 59Fe from TF prior to M.tb infection (endogenous
sources). M.tb 59Fe acquisition required viable bacteria and
was similar from exogenous and endogenous sources at 24 h and
greater from exogenous Fe at 48 h. Interferon-g treatment of
MDM reduced 59Fe uptake from TF 51% and TF receptor expression
34%. Despite this, intraphagosomal M.tb Fe acquisition in
IFN-g treated cells was decreased by only 30%. Macrophages
from hereditary hemochromatosis patients have altered Fe
metabolism. Intracellular M.tb acquired markedly less Fe in
MDM from these individuals than in MDM from healthy donors
regardless of the Fe source (exogenous and endogenous): 36 +/-
3.8% and 17 +/- 9.6% of control, respectively. Thus,
intraphagosomal M.tb can acquire Fe from both extracellular TF
and endogenous macrophage sources. Acquisition of Fe from
macrophage cytoplasmic Fe pools may be critical for the
intracellular growth of M.tb. This acquisition is altered by
IFN-g treatment to a small extent, but is markedly reduced in
macrophages from hemochromatosis patients.

PMID: 12399453

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