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Chlamydophila pneumoniae changes iron homeostasis in infected tissues

Marie Edvinsson1, Peter Frisk, Kerstin Boman

  • 1Department of Medical Sciences, Infectious Diseases, Uppsala University Hospital, 75185 Uppsala, Sweden. marie.edvinsson@medsci.uu.se

International Journal of Medical Microbiology : IJMM
|April 26, 2008
PubMed

Insights

Bacterial infections like Chlamydophila pneumoniae alter iron (Fe) levels by increasing hepcidin and DMT1, causing Fe redistribution to infected tissues, not affecting intestinal Fe uptake.

Area of Science:

  • Microbiology
  • Immunology
  • Nutritional Science

Background:

  • Bacteria require iron (Fe) for growth.
  • The impact of bacterial infections on gastrointestinal trace element uptake remains unclear.

Purpose of the Study:

  • To investigate how Chlamydophila pneumoniae infection affects hepcidin gene expression, divalent metal transporter 1 (DMT1) content, and iron (Fe) levels in mice.
  • To determine if infection influences trace element redistribution and body homeostasis.

Main Methods:

  • Chlamydophila pneumoniae infection model in C57BL/6J mice.
  • Real-time PCR for bacterial DNA, mRNA, and hepcidin.
  • Western blot for DMT1.
  • ICP-MS for trace element analysis (Fe, Cu, Zn).
  • Serum Cu/Zn ratio as an infection marker.

Main Results:

  • C. pneumoniae DNA detected in the liver, with viable bacteria peaking on day 8.
  • Increased hepcidin expression on days 2 and 5; increased liver DMT1 on day 8.
  • Serum Fe decreased, liver Fe increased, and intestinal Fe remained unchanged.
  • Serum Cu/Zn ratio peaked on day 5, indicating infection.

Conclusions:

  • C. pneumoniae infection causes Fe redistribution to infected liver tissue.
  • Increased hepcidin and DMT1 contribute to altered Fe homeostasis during infection.
  • Intestinal Fe uptake is not significantly affected despite systemic Fe changes.

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