痤疮丙酸杆菌通过 NF-κB 通路促进 MIF 表达诱导软骨终板退变。
Propionibacterium acnes induces cartilaginous endplate degeneration by promoting MIF expression via the NF-κB pathway.
机构信息
Department of Anesthesiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, 310016, China.
Department of Anesthesiology, Ningbo Yinzhou No. 2 Hospital, Ningbo, 315100, China.
出版信息
J Orthop Surg Res. 2020 Jun 9;15(1):213. doi: 10.1186/s13018-020-01714-6.
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.
背景
痤疮丙酸杆菌（P. acnes）是一种新型的致病因素，可导致软骨终板（CEP）退化。然而，P. acnes 诱导 CEP 退化的潜在机制尚不清楚。本研究旨在探讨 P. acnes 诱导的 CEP 退化的潜在机制。
方法
我们首先通过免疫组织化学法检测退变的人 CEP 样本中 MIF 的表达。我们建立了 P. acnes 诱导的大鼠模型，并通过免疫组织化学法检测 MIF 的表达。此外，我们通过 Western blot 和逆转录定量聚合酶链反应（RT-qPCR）研究了 P. acnes 诱导的 CEP 细胞退化的机制。
结果
与正常的人 CEP 相比，退变的人 CEP 中 MIF 的表达增加。在大鼠模型中，P. acnes 诱导 CEP 退化并显著上调 MIF 的表达。更重要的是，我们揭示了 P. acnes 诱导的大鼠 CEP 细胞退化的潜在机制。首先，P. acnes 以浓度依赖性方式诱导 MIF 的表达。然后，MIF 上调 MMP-13 的表达并促进 IL-6 和 IL-1β 的分泌。最后，P. acnes 可能通过 NF-κB 通路而不是 ERK1/2 通路促进 MIF 表达。
结论
P. acnes 通过 NF-κB 通路诱导 MIF 表达可能是 CEP 退化的潜在机制。
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