Journal of Orthopaedic Surgery and Research (Jun 2020)

Propionibacterium acnes induces cartilaginous endplate degeneration by promoting MIF expression via the NF-κB pathway

  • Ying Zhang,
  • Yuting Wang,
  • Yanyan Yuan,
  • Yeting Lin,
  • Binbin Lin,
  • Haiyan Zhou

DOI
https://doi.org/10.1186/s13018-020-01714-6
Journal volume & issue
Vol. 15, no. 1
pp. 1 – 10

Abstract

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Abstract Background Propionibacterium acnes (P. acnes) is a novel pathogenic factor that contributes to cartilaginous endplate (CEP) degeneration. However, the underlying mechanism of P. acnes-induced CEP degeneration remains unclear. The objective of this study is to investigate the underlying mechanism of P. acnes-induced CEP degeneration. Methods We first examined MIF expression in degenerated human CEP samples by immunohistochemistry. We developed a P. acnes-induced rat model and detected MIF expression using immunohistochemistry. Additionally, we investigated the mechanism of P. acnes-induced CEP degeneration in CEP cells using western blotting and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Results We found that compared with the normal human CEP, the expression of MIF was increased in the degenerated human CEP. In a rat model, P. acnes induced CEP degeneration and upregulated MIF expression significantly. More importantly, we revealed the underlying mechanism of P. acnes-induced CEP degeneration in the rat CEP cells. Firstly, P. acnes induced the expression of MIF in a concentration-dependent manner. Then, MIF upregulated the expression of MMP-13 and promoted the secretion of IL-6 and IL-1β. Finally, P. acnes may promote MIF expression via NF-κB pathway rather than ERK1/2 pathway. Conclusion P. acnes-induced MIF expression via NF-κB pathway may be the underlying mechanism of CEP degeneration.

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