Previously, we proposed the hypothesis that similarities in the inflammatory response observed in acne vulgaris and degenerative disc disease (DDD), especially the central role of interleukin (IL)-1β, may be further evidence of the role of the anaerobic bacterium Cutibacterium (previously Propionibacterium) acnes in the underlying aetiology of disc degeneration. To investigate this, we examined the upregulation of IL-1β, and other known IL-1β-induced inflammatory markers and neurotrophic factors, from nucleus-pulposus-derived disc cells infected in vitro with C. acnes for up to 48 h. Upon infection, significant upregulation of IL-1β, alongside IL-6, IL-8, chemokine (C-C motif) ligand 3 (CCL3), chemokine (C-C motif) ligand 4 (CCL4), nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), was observed with cells isolated from the degenerative discs of eight patients versus non-infected controls. Expression levels did, however, depend on gene target, multiplicity and period of infection and, notably, donor response. Pre-treatment of cells with clindamycin prior to infection significantly reduced the production of pro-inflammatory mediators. This study confirms that C. acnes can stimulate the expression of IL-1β and other host molecules previously associated with pathological changes in disc tissue, including neo-innervation. While still controversial, the role of C. acnes in DDD remains biologically credible, and its ability to cause disease likely reflects a combination of factors, particularly individualised response to infection.

• Keywords
• Cutibacterium acnes, co-culture, disc cells, gene expression, inflammation, intracellular, neurotrophic factors,
• MeSH
• Intervertebral Disc Degeneration genetics   microbiology   MeSH
• Adult MeSH
• Host-Pathogen Interactions MeSH
• Interleukin-1beta genetics   MeSH
• Cells, Cultured MeSH
• Middle Aged MeSH
• Humans MeSH
• Intervertebral Disc metabolism   microbiology   MeSH
• Nerve Growth Factors genetics   MeSH
• Propionibacterium acnes physiology   MeSH
• Up-Regulation MeSH
• Inflammation genetics   microbiology   MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• Interleukin-1beta MeSH
• Nerve Growth Factors MeSH