Periodontopathic Bacterium Fusobacterium nucleatum Affects Matrix Metalloproteinase-9 Expression in Human Alveolar Epithelial Cells and Mouse Lung
Periodontopathic Bacterium Fusobacterium nucleatum Affects Matrix Metalloproteinase-9 Expression in Human Alveolar Epithelial Cells and Mouse Lung
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DOI：
10.21873/invivo.12749
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发表时间：
2022
期刊：
影响因子：
2.3
通讯作者：
Ryuta Suzuki;Noriaki Kamio;Kozue Sugimoto;S. Maruoka;Y. Gon;T. Kaneko;Y. Yonehara;K. Imai
中科院分区：
文献类型：
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作者：
Ryuta Suzuki;Noriaki Kamio;Kozue Sugimoto;S. Maruoka;Y. Gon;T. Kaneko;Y. Yonehara;K. Imai
背景/目的：尽管有证据表明肺部疾病与牙周病细菌有关，但其分子机制仍不清楚。基质金属蛋白酶-9(MMP9)在肺炎、慢性阻塞性肺疾病和哮喘中起重要作用；因此，我们研究了核梭杆菌对小鼠肺和A549人肺泡上皮细胞MMP9表达的影响。材料和方法：将热灭活的核盘藻接种于小鼠气管内或加入A549细胞培养中。用实时定量聚合酶链式反应和免疫印迹法检测MMP9的表达。检测丝裂原活化蛋白激酶(MAPK)和核因子-κB(NF-κB)在MMP9表达中的作用。结果：核盘藻可诱导小鼠肺和支气管肺泡灌洗液中MMP9的表达。在A549细胞中，核颤菌以密度依赖的方式诱导MMP9蛋白和mR NA的产生，这一作用可被细胞外调节蛋白1/2和核因子κB的抑制剂抑制，但不能抑制p38和Jun N末端蛋白激酶的产生。结论：核假单胞菌可能通过细胞外调节的激酶1/2和核因子κB的激活而表达MMP9，从而参与肺部疾病的发生。
Background/Aim: Despite evidence of an association between pulmonary diseases and periodontopathic bacteria, the molecular mechanisms remain unknown. Matrix metalloproteinase-9 (MMP9) plays important roles in pneumonia, chronic obstructive pulmonary disease, and asthma; therefore, we assessed the effects of Fusobacterium nucleatum on MMP9 expression in mouse lung and A549 human alveolar epithelial cells. Materials and Methods: Heat-killed F. nucleatum was administered to the trachea of mice or added to A549 cell cultures. MMP9 expression was determined using real-time PCR and western blotting. The involvement of mitogen-activated protein kinases (MAPKs) and nuclear factor-κB (NF-κB) in MMP9 expression was examined. Results: F. nucleatum induced expression of MMP9 in mouse lung and bronchoalveolar lavage fluid. In A549 cells, F. nucleatum induced production of MMP9 protein and mRNA in a density-dependent manner; this was inhibited by inhibitors of extracellular-regulated kinase 1/2 and NF-κB, but not of p38 and Jun N-terminal protein kinase. Conclusion: F. nucleatum may contribute to the onset of pulmonary diseases via MMP9 expression through extracellular-regulated kinase 1/2 and NF-κB activation.