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Research article - Peer-reviewed, 2008

Chlamydophila pneumoniae changes iron homeostasis in infected tissues

Edvinsson, Marie; Frisk, Peter; Boman, Kerstin; Tallkvist, Jonas; Ilback, Nils-Gunnar

Abstract

Many bacteria, including Chlamydophila pneumoniae (C pneumoniae), are dependent on iron (Fe) for their growth. However, it is not known whether bacterial infections affect gastrointestinal uptake and uptake of trace elements in infected tissues. A human C. pneumoniae strain adapted to C57BL/6J mice was used to study hepcidin gene expression in the liver and divalent metal transporter 1 (DMT1) content in the liver and intestine and whether Fe is concomitantly changed in serum. liver, and intestine. The copper/zinc (Cu/Zn) ratio in the serum was used as a marker for infection. Bacterial DNA, mRNA, and hepcidin were measured by real-time PCR, DMT1 by Western blot, and trace elements by ICP-MS on days 2, 5, and 8 of the infection. C pneumoniae DNA was Found in the liver on all days but the number of viable bacteria peaked on day 8. Hepcidin expression increased on days 2 and 5, whereas DMT1 content in the liver increased on day 8. Fe decreased in serum. increased in the liver but was not changed in the Intestine during the disease. In the serum. the Cu/Zn ratio peaked on day 5. The peak of viable bacteria in the liver was associated with increased DMT1 and Fe contents and increased hepcidin expression, but this did not affect intestinal Fe uptake. Thus, growth of C pneumoniae in tissues parallels a redistribution of Fe to those tissues resulting, in a changed body homeostasis of Fe. (C) 2008 Elsevier GmbH. All rights reserved.

Keywords

Chlamydophila pneumonia; Chlamydia pneumoniae; DMT1; Hepcidin; Iron; Liver

Published in

International Journal of Medical Microbiology
2008, Volume: 298, number: 7-8, pages: 635-44

    SLU Authors

    UKÄ Subject classification

    Animal and Dairy Science
    Veterinary Science
    Food Science

    Publication Identifiers

    DOI: https://doi.org/10.1016/j.ijmm.2008.01.014

    Permanent link to this page (URI)

    https://res.slu.se/id/publ/20154