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Anti-lactoferrin toxicity, elevated iron and susceptibility to tuberculosis infection?
Journal
Medical
Hypotheses
Authors
Mark Purdey from Elworthy, Taunton, Somerset
Abstract
Anti-lactoferrin toxicity and elevated iron: The environmental prerequisites
which activate susceptibility to tuberculosis infection?
The maintenance and multiplication of Mycobacteria tuberculosis (TB) and many
other species of parasitic pathogen are dependent to varying, largely
unidentified degrees upon a source of free iron within the host tissues. To
combat these infections, the mammalian biosystem expresses an iron binding
exocrine protein, lactoferrin, which scavenges and competes for free iron,
thereby starving the parasite of its vital iron supply. TB mycobacteria are
naturally endemic in the external environment, and once a latent, low level TB
infection is established within the host tissues, a full blown proliferation of
the mycobacteria population can be activated as soon as the levels of free iron
are elevated within the host tissues. The increase in iron can be induced by
several environmental and/or eco-genetic prerequisites that operate either
singly or in a synergistic combination; factors such as iron rich water/foods,
increased iron uptake/retention in the host tissues or an environmental/genetic
induced reduction in the turn over of iron binding lactoferrin mediated immune
defence against TB. Susceptibility to the full blown proliferation of TB
pathogenesis is markedly increased as a result. This paper proposes that the
recent dramatic increase in the incidence of bovine/badger TB across the UK can
be correlated to the overall increase in acidification of the agricultural
ecosystem, which, in turn, has induced a substantial elevation of soluble iron
within the farm foodchain, thereby exacerbating susceptibility to TB infection
within any mammalian species that is dependent upon these high iron ecosystems.
The problem is further compounded by the routine use of ‘anti-lactoferrin’
levamisole based cattle wormers, which ‘sensitise’ the levamisole’s target
receptors, thereby down regulating the secretion of the iron binding lactoferrin
molecule, which causes a reduction in the host’s main line of defence against TB
infection.
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