Chlamydia trachomatis alters iron-regulatory protein-1 binding capacity and modulates cellular iron homeostasis in HeLa-229 cells

J Biomed Biotechnol. 2009:2009:342032. doi: 10.1155/2009/342032. Epub 2009 Aug 16.

Abstract

Chlamydia trachomatis (CT) is the leading cause of diseases related to reproductive health and iron plays important role in chlamydial pathogenesis. Iron homeostasis in chlamydia-infected cells is not clear thus far. This study shows that expression of the transferrin receptor (TfR) is downregulated, whereas expression of the ferritin heavy chain is upregulated in CT-infected HeLa-229 cells. Expression of iron-regulatory protein (IRP)-1 predominates over IRP-2 in infected cells. In infected cells, attenuated binding activity of IRP-iron responsive elements (IREs) is observed using the electrophoretic mobility-shift assay. These results suggest that iron homeostasis is modulated in CT-infected HeLa cells at the interface of acquisition and commensal use of iron.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Apoferritins / biosynthesis
  • Apoferritins / genetics
  • Apoferritins / metabolism
  • Chlamydia Infections / genetics
  • Chlamydia Infections / metabolism*
  • Chlamydia trachomatis / metabolism*
  • Down-Regulation
  • HeLa Cells
  • Humans
  • Iron / metabolism*
  • Iron Regulatory Protein 1 / biosynthesis
  • Iron Regulatory Protein 1 / genetics
  • Iron Regulatory Protein 1 / metabolism*
  • Iron Regulatory Protein 2 / biosynthesis
  • Iron Regulatory Protein 2 / genetics
  • Iron Regulatory Protein 2 / metabolism
  • Protein Binding
  • Receptors, Transferrin / biosynthesis
  • Receptors, Transferrin / genetics
  • Receptors, Transferrin / metabolism
  • Response Elements
  • Up-Regulation

Substances

  • Receptors, Transferrin
  • Apoferritins
  • Iron
  • Iron Regulatory Protein 1
  • Iron Regulatory Protein 2