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Objective <p>Osteoarthritis (OA) is one of the leading causes of disability in the aging population. While about 10% of the adult population is affected by OA, there is to date no curative treatment and joint replacement surgery remains the only option for treating end-stage OA. Previous studies found elevated levels of the chemokine C-X-C motif ligand 9 (CXCL9) in the synovial fluid of OA knees. However, the exact role of CXCL9 in OA progression is still unknown.</p> Methods <p>Female wild-type and <i>Cxcl9</i>-deficient mice were challenged with a unilateral anterior cruciate ligament transection (ACLT). Joint destruction in early and late stages of experimental OA was assessed using micro-CT scanning, histological scoring, histomorphometry, and gene expression analysis.</p> Results <p>Inactivation of <i>Cxcl9</i> protected from cartilage destruction and osteophyte formation in post-traumatic OA in mice. Similarly, indices of joint inflammation including synovitis and expression of pro-inflammatory interleukin-1beta were reduced in OA knees of <i>Cxcl9</i>-deficient mice. However, bone erosion and pathophysiological changes in the subchondral bone compartment remained unaffected in <i>Cxcl9</i>-deficient mice with experimental OA.</p> Conclusion <p>Our results point towards a pro-inflammatory role of CXCL9 in OA and identify a potential new target for the pharmacological treatment of OA.</p>

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Cxcl9-deficiency attenuates the progression of post-traumatic osteoarthritis in mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年3月6日

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  • Antonia Donat,
  • Weixin Xie,
  • Shan Jiang,
  • Laura Janina Brylka,
  • Thorsten Schinke,
  • Tim Rolvien,
  • Karl-Heinz Frosch,
  • Anke Baranowsky,
  • Johannes Keller

摘要

Objective

Osteoarthritis (OA) is one of the leading causes of disability in the aging population. While about 10% of the adult population is affected by OA, there is to date no curative treatment and joint replacement surgery remains the only option for treating end-stage OA. Previous studies found elevated levels of the chemokine C-X-C motif ligand 9 (CXCL9) in the synovial fluid of OA knees. However, the exact role of CXCL9 in OA progression is still unknown.

Methods

Female wild-type and Cxcl9-deficient mice were challenged with a unilateral anterior cruciate ligament transection (ACLT). Joint destruction in early and late stages of experimental OA was assessed using micro-CT scanning, histological scoring, histomorphometry, and gene expression analysis.

Results

Inactivation of Cxcl9 protected from cartilage destruction and osteophyte formation in post-traumatic OA in mice. Similarly, indices of joint inflammation including synovitis and expression of pro-inflammatory interleukin-1beta were reduced in OA knees of Cxcl9-deficient mice. However, bone erosion and pathophysiological changes in the subchondral bone compartment remained unaffected in Cxcl9-deficient mice with experimental OA.

Conclusion

Our results point towards a pro-inflammatory role of CXCL9 in OA and identify a potential new target for the pharmacological treatment of OA.