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INF-γ encoding plasmid administration triggers bone loss and disrupts bone marrow microenvironment.

Dimitrios Agas1, Guilherme Gusmão Silva2, Fulvio Laus1

  • 1School of Bioscience and Veterinary MedicineUniversity of Camerino, Camerino, Italy.

The Journal of Endocrinology
|December 3, 2016
PubMed
Summary

Increased interferon-gamma (IFN-γ) synthesis, even without disease, impairs bone health. This study investigated the effects of an IFN-γ encoding plasmid (pIFN-γ) on bone loss and marrow changes.

Keywords:
INF-γbone lossbone marrowplasmid DNA

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Area of Science:

  • Bone Biology
  • Immunology
  • Skeletal Homeostasis

Background:

  • Interferon-gamma (IFN-γ) is a cytokine in the bone microenvironment with a known role in bone remodeling.
  • Previous studies on recombinant IFN-γ effects on bone loss have yielded contradictory results.
  • The specific role of IFN-γ encoding plasmid (pIFN-γ) in skeletal homeostasis remains unclear.

Purpose of the Study:

  • To investigate the effects of pIFN-γ on bone microarchitecture and bone mineral density (BMD) in an ovariectomy-induced osteopenia mouse model.
  • To assess the impact of pIFN-γ on bone marrow cellularity and mesenchymal stem cell (MSC) differentiation.
  • To determine if increased IFN-γ synthesis alone can induce inflammatory and catabolic bone responses.

Main Methods:

  • Ovariectomy and sham surgeries in mice.
  • Intra-bone marrow injection of pIFN-γ.
  • Analysis of bone mineral density (BMD) and bone microarchitecture.
  • Histological examination of bone and bone marrow.
  • Assessment of MSC commitment to osteoblast differentiation via osterix-positive (Osx+) cell counts.
  • Evaluation of pro-inflammatory cytokine release and CXCL12 cell distribution.

Main Results:

  • Ovariectomy significantly decreased BMD.
  • pIFN-γ injection led to pathological bone and bone marrow phenotypes in both ovariectomized and sham-operated mice.
  • Disrupted bone microarchitecture, increased pro-inflammatory cytokines, and impaired MSC osteogenic commitment were observed.
  • Reduction and redistribution of CXCL12 cells correlated with bone marrow alterations.

Conclusions:

  • Increased IFN-γ synthesis in the bone marrow is sufficient to induce inflammatory and catabolic responses, even without predisposing pathological conditions.
  • pIFN-γ administration negatively impacts skeletal homeostasis by disrupting bone microarchitecture and impairing osteoblast differentiation.
  • The findings raise safety concerns regarding the use of pIFN-γ as a vaccine adjuvant due to its potential to induce bone pathology.