Pro-Inflammatory and Neurotrophic Factor Responses of Cells Derived from Degenerative Human Intervertebral Discs to the Opportunistic Pathogen Cutibacterium acnes

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