Chlamydia pneumoniae infection results in generalized bone loss in mice

Microbes Infect. 2008 Aug-Sep;10(10-11):1175-81. doi: 10.1016/j.micinf.2008.06.010. Epub 2008 Jun 29.

Abstract

Osteoporosis is associated with a general bone loss. Whether infections could contribute to osteoporosis is not known. Chlamydia pneumoniae causes chronic infections and produces potentially bone resorptive cytokines. The effect of C. pneumoniae infection was investigated in vivo in 10-week old mice (c57BL/6) and in vitro in the human osteoblast-like cell line hFOB 1.19 (hFOB). Bone mineral density (BMD) was measured before and 16 days after infection. C. pneumoniae-infected mice had decreased (p<0.05) total and subcortical BMD at the distal femur and proximal tibia compared with controls, but no body-weight gain differences. IL-6 (56 vs. 39pg/mL, p=0.02) and IL-1beta (11 vs. 0pg/mL, p=0.003) levels in sera, and CD3(+) T-cells (p=0.04) were higher in infected mice compared with controls. In vitro, hFOB infected with C. pneumoniae was associated with increased IL-6 (p=0.01) and RANKL (p<0.05) mRNA expression; additionally, IL-6 secretion increased in a dose-dependent manner (p<0.05). In summary, mice infected with C. pneumoniae had generalized bone loss associated with increased IL-6 and IL-1. In addition, C. pneumoniae established an infection in an osteoblast cell line in vitro with similar cytokine profiles as those in vivo, supporting a causal linkage.

MeSH terms

  • Animals
  • Bone Density*
  • Bone Diseases, Metabolic / etiology*
  • Bone Diseases, Metabolic / immunology
  • Bone Diseases, Metabolic / metabolism
  • Calcification, Physiologic*
  • Cell Line
  • Cell Proliferation
  • Chlamydophila Infections / complications
  • Chlamydophila Infections / microbiology
  • Chlamydophila Infections / physiopathology*
  • Chlamydophila pneumoniae / pathogenicity*
  • Femur
  • Humans
  • Interleukins / genetics
  • Interleukins / immunology
  • Interleukins / metabolism
  • Male
  • Mice
  • Osteoblasts / immunology
  • Osteoblasts / metabolism
  • Osteoblasts / microbiology*
  • Osteoclasts / physiology
  • RANK Ligand / genetics
  • RANK Ligand / immunology
  • RANK Ligand / metabolism
  • Tibia
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / immunology
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Interleukins
  • RANK Ligand
  • TNFSF11 protein, human
  • Tumor Necrosis Factor-alpha