Although cervical intervertebral disc (IVD) degeneration is closely associated with neck pain, its cause remains unclear. In this study, an animal model of cervical disc degeneration and discogenic neck pain induced by a low concentration of Propionibacterium acnes (P. acnes-L) is investigated to explore the possible mechanisms of cervical discogenic pain. Cervical IVD degeneration and discitis was induced in 8-week-old male rats in C3–C6 IVDs through the anterior intervertebral puncture with intradiscal injections of low and high concentrations of P. acnes (P. acnes-L, n = 20 and P. acnes-H, n = 15) or Staphylococcus aureus (S. aureus, n = 15), compared to control (injection with PBS, n = 20). The structural changes in the cervical IVD using micro-CT, histological evaluation, and gene expression assays after MRI scans at 2 and 6 weeks post-modeling. The P. acnes-L induced IVD degeneration model was assessed for cervical spine MRI, histological degeneration, pain-like behaviors (guarding behavior and forepaw von Frey), nerve fiber growth in the IVD endplate region, and DRG TNF-α and CGRP. IVD injection with P. acnes-L induced IVD degeneration with decreased IVD height and MRI T2 values. IVD injection with P. acnes-H and S. aureus both lead to discitis-like changes on T2-weighted MRI, trabecular bone remodeling on micro-CT, and osseous fusion after damage in the cartilage endplate adjacent to the injected IVD. Eventually, rats in the P. acnes-L group exhibited significant nociceptive hypersensitivity, nerve fiber ingrowth was observed in the IVD endplate region, inflammatory activity in the DRG was significantly increased compared to the control group, and the expression of the pain neurotransmitter CGRP was significantly upregulated. P. acnes-L was validated to induce cervical IVD degeneration and discogenic pain phenotype, while P. acnes-H induced was identified to resemble septic discitis comparable to those caused by S. aureus infection.

中文翻译：

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低浓度痤疮丙酸杆菌感染诱导颈椎间盘退变和椎间盘源性疼痛：体内动物研究


尽管颈椎间盘（IVD）退变与颈部疼痛密切相关，但其原因仍不清楚。本研究通过低浓度痤疮丙酸杆菌（P.acnes-L）诱导的颈椎间盘退变和椎间盘源性颈部疼痛动物模型进行研究，以探讨颈椎间盘源性疼痛的可能机制。通过前椎间穿刺并椎间盘内注射低浓度和高浓度的痤疮丙酸杆菌（P.acnes-L，n = 20 和 P.acnes-L，n = 20），在 C3-C6 IVD 中的 8 周龄雄性大鼠中诱导颈椎 IVD 退变和椎间盘炎。痤疮-H，n = 15）或金黄色葡萄球菌（S. aureus，n = 15），与对照（注射 PBS，n = 20）相比。在建模后 2 周和 6 周进行 MRI 扫描后，使用显微 CT、组织学评估和基因表达测定来观察宫颈 IVD 的结构变化。对痤疮丙酸杆菌-L 诱导的 IVD 变性模型进行了颈椎 MRI、组织学变性、疼痛样行为（守卫行为和前爪 von Frey）、IVD 终板区域神经纤维生长以及 DRG TNF-α 和 CGRP 的评估。 IVD 注射 P. acnes-L 诱导 IVD 变性，IVD 高度和 MRI T2 值降低。 IVD 注射痤疮丙酸杆菌-H 和金黄色葡萄球菌都会导致 T2 加权 MRI 上的椎间盘炎样变化、显微 CT 上的骨小梁重塑以及注射 IVD 附近的软骨终板损伤后的骨融合。最终，痤疮丙酸杆菌-L组大鼠表现出明显的伤害性超敏反应，IVD终板区域观察到神经纤维向内生长，背根神经节炎症活性较对照组显着增加，疼痛神经递质CGRP的表达量显着升高。显着上调。 P。 经验证，acnes-L 可以诱导宫颈 IVD 变性和椎间盘源性疼痛表型，而痤疮丙酸杆菌-H 诱导的脓毒症椎间盘炎被鉴定为与金黄色葡萄球菌感染引起的脓毒症椎间盘炎类似。