title: Chlamydia pneumoniae infection results in generalized bone loss in mice.
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.
authors.affiliation: Department of Molecular Biology, Umeå University, SE-90187, Umeå, Sweden.
authors.forename: Leslie
authors.initials: L
authors.lastname: Bailey
authors.forename: Patrik
authors.initials: P
authors.lastname: Engström
authors.forename: Anna
authors.initials: A
authors.lastname: Nordström
authors.forename: Sven
authors.initials: S
authors.lastname: Bergström
authors.forename: Anders
authors.initials: A
authors.lastname: Waldenström
authors.forename: Peter
authors.initials: P
authors.lastname: Nordström
mesh_terms: D000818:Animals; D015519:Bone Density; D001851:Bone Diseases, Metabolic / Q000209:etiology* / Q000276:immunology / Q000378:metabolism; D002113:Calcification, Physiologic; D002460:Cell Line; D049109:Cell Proliferation; D023521:Chlamydophila Infections / Q000150:complications / Q000382:microbiology / Q000503:physiopathology*; D016993:Chlamydophila pneumoniae / Q000472:pathogenicity*; D005269:Femur; D006801:Humans; D007378:Interleukins / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D008297:Male; D051379:Mice; D010006:Osteoblasts / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D010010:Osteoclasts / Q000502:physiology; D053245:RANK Ligand / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D013977:Tibia; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology / Q000378:metabolism
chemical_list: D007378:Interleukins; D053245:RANK Ligand; C505688:TNFSF11 protein, human; D014409:Tumor Necrosis Factor-alpha