(HOME) Subject: iron/chelate/bacteria

   
   Immunology 1998 Aug;94(4):488-95
   
Interferon-gamma-activated primary enterocytes inhibit Toxoplasma gondii
replication: a role for intracellular iron.

    Dimier IH, Bout DT
    
   CJF INSERM 93-09 'Immunologie des Maladies Infectieuses', Equipe
   associee INRA 'Immunologie Parasitaire', UFR des Sciences
   Pharmaceutiques, Tours, France.
   
   Toxoplasma gondii is an obligate intracellular parasite that infects a
   wide variety of nucleated cells in its numerous intermediate hosts
   including man. The oral route is the natural portal of entry of T.
   gondii. Ingested organisms are released from cysts or oocysts within
   the gastrointestinal tract and initially invade the intestinal
   epithelium. We show that T. gondii invades and proliferates in
   cultured primary rat enterocytes, obtained with an original procedure.
   Activation of the enterocytes with rat recombinant interferon-gamma
   (IFN-gamma) inhibits T. gondii replication, the inhibition being dose
   dependent. Neither nitrogen and oxygen derivatives nor tryptophan
   starvation appear to be involved in the inhibition of parasite
   replication by IFN-gamma. Experiments using Fe2+ salt, carrier and
   chelator indicate that intracellular T. gondii replication is iron
   dependent, suggesting that IFN-gamma-treated enterocytes inhibit T.
   gondii replication by limiting the availability of intracellular iron
   to the parasite. Our data show that enterocytes probably play a major
   role on mucosal surfaces as a first line of defence against this
   coccidia, and possibly other pathogens, through an immune mechanism.
   The results suggest that limiting the availability of iron could
   represent a broad antimicrobial mechanism through which the activated
   enterocytes exert control over intracellular pathogens.
   
   PMID: 9767436, UI: 98440381
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   Antimicrob Agents Chemother 1996 May;40(5):1298-1300
   
Trophozoite elimination in a rat model of Pneumocystis carinii pneumonia by
clinically achievable plasma deferoxamine concentrations.

    Merali S, Chin K, Grady RW, Clarkson AB Jr
    
   Department of Medical and Molecular Parasitology, New York University
   School of Medicine, New York 10016, USA.
   
   In a rat model of Pneumocystis carinii pneumonia, a 3-week infusion of
   deferoxamine producing concentrations in plasma of > or = 1.5
   micrograms m-1 eliminated the trophozoite life cycle stage. Since this
   concentration is well below that routinely achieved in patients
   treated for iron overload, deferoxamine has promise as a therapy for
   AIDS-associated P.carinii pneumonia.
   
   PMID: 8723489, UI: 96300560
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