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Yazhou Lin1,2, Guoqing Tang3, Yucheng Jiao1,2

  • 1Department of Orthopedics, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

Oxidative Medicine and Cellular Longevity
|September 14, 2018
PubMed
Summary

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This summary is machine-generated.

Propionibacterium acnes (P. acnes) drives intervertebral disc degeneration (IVDD) by increasing nitric oxide (NO) and prostaglandin (PGE2) via a reactive oxygen species (ROS) pathway. Inhibiting these pathways ameliorates IVDD, revealing a novel therapeutic target.

Area of Science:

  • Biomedical Science
  • Microbiology
  • Orthopedics

Background:

  • Propionibacterium acnes (P. acnes) is increasingly implicated in intervertebral disc degeneration (IVDD).
  • The precise molecular mechanisms linking P. acnes infection to IVDD pathogenesis remain incompletely understood.
  • Investigating the roles of inducible nitric oxide synthase (iNOS)/nitric oxide (NO) and cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) pathways is crucial.

Purpose of the Study:

  • To elucidate the mechanisms by which P. acnes contributes to IVDD.
  • To quantify the expression of iNOS/NO and COX-2/PGE2 in P. acnes-infected human intervertebral discs (IVDs).
  • To establish and validate a P. acnes-induced IVDD rat model to explore therapeutic interventions.

Main Methods:

  • Quantification of IVDD severity and iNOS/NO, COX-2/PGE2 expression in human IVDs.

Related Experiment Videos

  • Development of a P. acnes-induced IVDD rat model.
  • In vivo and in vitro experiments involving inhibition of iNOS/NO and COX-2/PGE2 pathways.
  • Analysis of the reactive oxygen species (ROS)-dependent NF-κB cascade and NADPH oxidase involvement.

    • Main Results:

    • P. acnes-positive human IVDs exhibited more severe degeneration with elevated iNOS/NO and COX-2/PGE2 activity compared to negative controls.
    • The P. acnes-induced IVDD rat model demonstrated that iNOS/NO and COX-2/PGE2 upregulation is essential for IVDD development.
    • Inhibition of iNOS/NO and COX-2/PGE2 significantly ameliorated IVDD, restoring aggrecan and collagen II expression.
    • P. acnes induced iNOS/NO and COX-2/PGE2 via a ROS-dependent NF-κB pathway, with NADPH oxidase playing a key role.

    Conclusions:

    • P. acnes is a significant factor in the pathology of IVDD.
    • The ROS-dependent NF-κB pathway, involving NADPH oxidase, mediates P. acnes-induced iNOS/NO and COX-2/PGE2 activation.
    • Targeting the iNOS/NO and COX-2/PGE2 pathways offers a promising therapeutic strategy for P. acnes-related IVDD.