Iron and the Risk of Infection / inflammation

Discussion in 'Food and nutrition' started by [email protected], Dec 28, 2005.

  1. 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
     
    Tags:


  2. One realizes that as one becomes more mature in ones thinking, as you have
    recently displayed, there are bound to be minor setbacks to progress.
    Please note that iron was not the cause of infection, recall the germ
    theory of disease, but iron is one of the factors that influence its
    process. It is best to never allow the dog/tail image to stray far from
    one's thinking and the way one phrases subject lines.
     
  3. <<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:
    [email protected] and [email protected]


    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
     
Loading...