Iron and the Risk of Infection
Jul 2005, Vol. 6, No. supplement 1: s-41-s-46
Fredric M. Pieracci
Department of Surgery, Weill Medical College of Cornell University, New
York, New York.
Dr. Philip S. Barie
Departments of Surgery and Public Health, Weill Medical College of
Cornell University, New York, New York.
Background: During bacterial infection, pathogen and host compete for
iron (Fe). The inflammatory response associated with infection shifts
Fe from the circulation into storage, resulting in hypoferremia and
iron-deficient erythropoiesis, and ultimately contributing to the
anemia of inflammation.
Methods: In this article, we review the mechanisms of Fe acquisition
and sequestration. Bacteria employ both membrane-bound transferrin
receptors and high-affinity iron-binding proteins called siderophores
to acquire Fe. Humans utilize the iron-binding proteins lactoferrin,
transferrin, and ferritin to move Fe away from sites of infection and
into storage. Synthesis and action of these proteins are regulated by
inflammatory cytokines.
Results: Iron overload leads to inhibition of IFN-?, TNF-a, IL-12, and
nitric oxide formation as well as impairment of macrophage, neutrophil,
and T-cell function. Injection of Fe into mice and rats markedly
increases the virulence of several pathogens. Studies in hemodialysis
patients have documented an association between infection and increased
ferritin concentration as a surrogate marker for Fe overload.
Conclusions: Humans respond to infection with inflammatory
cytokine-induced hypoferremia. This association, as well as the growing
literature linking Fe to both impaired immunity and heightened
microbial virulence, calls into question the value of Fe
supplementation during inflammation and infection.
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com
Man Is A Herbivore!
http://pages.ivillage.com/ironjustice/manisaherbivore
DEAD PEOPLE WALKING
http://pages.ivillage.com/ironjustice/deadpeoplewalking
<<snip>>
The intestinal mucosal cells are constantly exposed to unabsorbed iron
excess and oxidative stress
<<snip>>
http://tinyurl.com/a3ynu
<<snip>>
Dietary oxidative stress allows a normally benign coxsackievirus B3 to
convert to virulence
This is the first report of host nutrition affecting the genetic
sequence of a pathogen
<<snip>>
Abstract
Annual Review of Nutrition
Vol. 18: 93-116 (Volume publication date July 1998)
(doi:10.1146/annurev.nutr.18.1.93)
DIETARY OXIDATIVE STRESS AND THE POTENTIATION OF VIRAL INFECTION1
Melinda A. Beck and *Orville A. Levander*
Frank Porter Graham Child Development Center, University of North
Carolina, Chapel Hill, North Carolina 27599-8180;
Nutrient Requirements and Functions Laboratory, Beltsville Human
Nutrition Research Center, Beltsville, Maryland 20705-2350; e-mail:
melinda_b...@unc.edu and levan...@307.bhnrc.usda.gov
Oxidative stress is implicated in the pathogenesis of several viral
infections, including hepatitis, influenza, and AIDS. Dietary oxidative
stress due to either selenium or vitamin E deficiency increases cardiac
damage in mice infected with a myocarditic strain of coxsackievirus B3.
Such dietary oxidative stress also allows a normally benign (i.e.
amyocarditic) coxsackievirus B3 to convert to virulence and cause heart
damage. This conversion to virulence is due to a nucleotide sequence
change in the genome of the benign virus, which then resembles more
closely the nucleotide sequence of virulent strains. Although it has
been known for many years that poor nutrition can affect host response
to infection, this is the first report of host nutrition affecting the
genetic sequence of a pathogen. Further research is needed to determine
whether poor host nutrition plays any role in the emergence of new
viral diseases via alterations in the genotype of an infectious agent.
Who loves ya.
Tom
Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com
Man Is A Herbivore!
http://pages.ivillage.com/ironjustice/manisaherbivore
DEAD PEOPLE WALKING
http://pages.ivillage.com/ironjustice/deadpeoplewalking