Eur J Gastroenterol Hepatol 2000 Dec;12(12):1263-5
   
Role of iron in Helicobacter pylori: its influence in outer membrane protein
expression and in pathogenicity.

    Perez-Perez GI, Israel DA
    
   Department of Medicine, New York University, NY 10016, USA.
   guillermo.perez-perez@med.nyu.edu
   
   The acquisition of iron is a necessity for bacterial growth in
   Helicobacterpylori, as it is for other organisms. In addition, iron is
   a critical factor for the virulence of this organism. Therefore, it is
   not surprising that H. pylori isolates have the potential to express
   at least three major iron acquisition mechanisms. The association of
   H. pylori infection with host iron deficiency might indicate that the
   iron-scavenging systems play a role in the virulence of H. pylori.
   
   Publication Types:
     * Review
     * Review, tutorial
       
   PMID: 11192313, UI: 21031083
     _________________________________________________________________
   
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     _________________________________________________________________

   Am J Surg Pathol 1999 Oct;23(10):1241-7
   
Erosive injury to the upper gastrointestinal tract in patients receiving iron
medication: an underrecognized entity.

    Abraham SC, Yardley JH, Wu TT
    
   Department of Pathology, The Johns Hopkins University School of
   Medicine, Baltimore, MD 21205-2196, USA.
   
   Severe gastrointestinal necrosis and strictures after an iron overdose
   are well described. However, mucosal injury in patients receiving
   therapeutic iron has received only scant recognition despite its wide
   use. We studied the clinical and histologic features of 36 upper
   gastrointestinal tract biopsies from 33 patients (24 gastric, 9
   esophageal, 1 gastroesophageal junction, and 2 duodenal) containing
   characteristic brown crystalline iron material, and evaluated the
   amount and tissue distribution of the iron. In addition, we
   investigated the prevalence of iron-associated mucosal injury in upper
   gastrointestinal endoscopic examinations. The majority of the biopsies
   (32 of 36, 89%) contained luminal crystalline iron adjacent to the
   surface epithelium or admixed with luminal fibrinoinflammatory
   exudate. Thirty biopsies (83%) showed crystalline iron deposition in
   the lamina propria, either covered by an intact epithelium, subjacent
   to small superficial erosions, or admixed with granulation tissue.
   Three biopsies (8%) demonstrated iron-containing thrombi in mucosal
   blood vessels. Erosive or ulcerative mucosal injury was present in 30
   of 36 biopsies (83%). The amount of iron accumulation in cases with
   mucosal injury was greater than in cases without mucosal injury (mean
   grades, 2.4+ vs. 1.3+ on a 1+ to 3+ scale; p = 0.002). Iron medication
   was confirmed in 25 of 33 patients (76%) 22 patients were receiving
   ferrous sulfate. Approximately half of the patients (17 of 33, 51%)
   also had underlying infectious, mechanical, toxic, or systemic medical
   conditions that could have initiated or exacerbated tissue injury.
   Crystalline iron deposition was found in 0.9% of upper
   gastrointestinal endoscopic examinations (12 of 1,300), and iron
   medication-associated erosive mucosal injury was present in 0.7% (9 of
   1,300). These results indicate that crystalline iron deposition in the
   upper gastrointestinal tract is not uncommon. It can induce or
   exacerbate a distinctive histologic pattern of erosive mucosal injury,
   especially in patients with associated upper gastrointestinal
   disorders. Recognition of this pattern by pathologists and its
   communication to clinicians may aid in optimizing therapy.
   
   PMID: 10524525, UI: 99452156
     _________________________________________________________________

Subject: Iron and bacteria


    ______________

  

   J Clin Invest 61: 1428-40 (1978)[78194498]

The critical role of iron in host-bacterial interactions.



    S. M. Payne & R. A. Finkelstein



   The ability of potential pathogens to acquire iron in a host is an
   important determinant of both their virulence and the nature of the
   infection produced. Virulent gram-negative bacteria are capable of
   acquiring sufficient iron from the host because their virulence (for
   chick embryos) is unaffected by exogenous iron. Avirulent mutants
   which are apparently limited in their ability to acquire iron could be
   isolated from the virulent strains. The lethality of these mutants was
   significantly enhanced by exogenous iron. Reduction of the relatively
   high serum iron saturation of chick embryos (to levels more closely
   approximating those in man) by pretreatment with iron-binding proteins
   or endotoxin inhibits the lethality of some virulent bacteria. Those
   bacteria whose virulence was reduced include the Shigella, Vibrio
   cholerae and strains of Neisseria gonorrhoeae, all of which are
   nondisseminating pathogens in the normal human host. Pathogens which
   produce septicemic and disseminating infections such as Neisseria
   meningitidis, Haemophilus influenzae type B, Escherichia coli
   possessing K-1 antigen, Pseudomonas aeruginosa and Salmonella
   typhimurium and disseminating strains of N. gonorrhoeae were, in
   general, unaffected by reduced serum iron saturation. These
   disseminating bacteria appeared to produce greater quantities of
   compounds (siderophores) which stimulated microbial growth in low-iron
   media than did the nondisseminating pathogens. Thus, the gram-negative
   bacteria tested can be divided into four major classes according to
   their responses to modifications in iron levels in the chick embryo
   model and these results correlate with the nature of the infections
   which they typically produce in man.

   MeSH Terms:
     * Animal
     * Bacteria/drug effects
     * Bacteria/metabolism
     * Bacteria/pathogenicity
     * Bacterial Infections/immunology
     * Bacterial Infections/metabolism
     * Chick Embryo
     * Conalbumin/pharmacology
     * Iron/metabolism
     * Iron/pharmacology
     * Iron Chelates/metabolism
     * Support, U.S. Gov't, P.H.S.


     _________________________________________________________________


Subject: colitis and iron

   
   Inflamm Bowel Dis 1999 Nov;5(4):253-61
   
Deferiprone, an oral iron chelator, ameliorates experimental colitis and
gastric ulceration in rats.

    Ablin J, Shalev O, Okon E, Karmeli F, Rachmilewitz D
    
   Department of Medicine, Hadassah University Hospital, Mount Scopus,
   Israel.
   
   [Medline record in process]
   
   Iron is pivotal is producing tissue-damaging reactive oxygen
   metabolites. Our aim is to determine the antiinflammatory activity of
   deferiprone, an oral iron chelator, in experimental colitis and
   gastritis. Colitis was induced by intraceccal administration of 2 ml
   5% acetic acid or by intracolonic administration of 0.1 ml 3%
   iodoacetamide, with or without cotreatment with deferiprone. Gastritis
   was induced by intragastric administration of ethanol or hydrochloric
   acid (HCl) and by subcutaneous injection of indomethacin, with and
   without deferiprone. Rats were killed 24 hours after acetic acid and
   iodoacetamide, 30 minutes after ethanol, one hour after HCl, and three
   hours after indomethacin administration. The colon or stomach was
   isolated, macroscopic damage was measured, and mucosal samples were
   obtained for determination of eicosanoid generation, myeloperoxidase
   (MPO), and nitric oxide synthase (NOS) activities. Deferiprone
   decreased iodoacetamide and acetic acid-induced macroscopic colonic
   damage by 67% and 69%, respectively, and macroscopic gastric damage by
   91%, 68%, and 46% induced by ethanol, HCl, and indomethacin,
   respectively. The effect of deferiprone was accompanied by significant
   decrease in colonic and gastric, MPO and NOS activities, and colonic
   prostaglandin E2 (PGE2) generation, in acetic acid, ethanol, and
   indomethacin models, whereas in the iodoacetamide and HCl models
   atte (HOME) nuation of the decrease in PGE2 generation was seen. Deferiprone
   is protective in experimental colitis and gastritis, probably due to
   decreased production of iron-dependent oxygen-free radicals. Oral iron
   chelators may constitute a novel approach to ameliorate
   gastrointestinal inflammatory disorders.
   
   PMID: 10579118, UI: 20046080
     _________________________________________________________________
   
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