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牙龈卟啉单胞菌脂多糖的不均一脂质 A 结构对人牙龈成纤维细胞基质金属蛋白酶-3 的表达和调节具有关键性影响。

The expression and regulation of matrix metalloproteinase-3 is critically modulated by Porphyromonas gingivalis lipopolysaccharide with heterogeneous lipid A structures in human gingival fibroblasts.

机构信息

Faculty of Dentistry, Periodontology, The University of Hong Kong, Hong Kong SAR, China.

出版信息

BMC Microbiol. 2013 Mar 30;13:73. doi: 10.1186/1471-2180-13-73.

DOI:10.1186/1471-2180-13-73
PMID:23548063
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3623786/
Abstract

BACKGROUND

Porphyromonas gingivalis lipopolysaccharide (LPS) is a crucial virulence factor strongly associated with chronic periodontitis which is the primary cause of tooth loss in adults. It exhibits remarkable heterogeneity containing tetra-(LPS(1435/1449)) and penta-(LPS(1690)) acylated lipid A structures. Human gingival fibroblasts (HGFs) as the main resident cells of human gingiva play a key role in regulating matrix metalloproteinases (MMPs) and contribute to periodontal homeostasis. This study investigated the expression and regulation of MMPs1-3 and tissue inhibitors of MMP-1 (TIMP-1) in HGFs in response to P. gingivalis LPS(1435/1449) and LPS(1690) and hexa-acylated E. coli LPS as a reference. The expression of MMPs 1-3 and TIMP-1 was evaluated by real-time PCR and ELISA.

RESULTS

The MMP-3 mRNA and protein were highly upregulated in P. gingivalis LPS(1690)- and E. coli LPS-treated cells, whereas no induction was observed in P. gingivalis LPS(1435/1449)-treated cells. On the contrary, the expression of MMP-1 and -2 was not significantly affected by P. gingivalis LPS lipid A heterogeneity. The TIMP-1 mRNA was upregulated in P. gingivalis LPS(1435/1449)- and E. coli LPS-treated cells. Next, signal transduction pathways involved in P. gingivalis LPS-induced expression of MMP-3 were examined by blocking assays. Blockage of p38 MAPK and ERK significantly inhibited P. gingivalis LPS(1690)-induced MMP-3 expression in HGFs.

CONCLUSION

The present findings suggest that the heterogeneous lipid A structures of P. gingivalis LPS differentially modulate the expression of MMP-3 in HGFs, which may play a role in periodontal pathogenesis.

摘要

背景

牙龈卟啉单胞菌脂多糖(LPS)是一种重要的毒力因子,与慢性牙周炎密切相关,后者是成年人牙齿丧失的主要原因。它表现出显著的异质性,包含四-(LPS(1435/1449))和五-(LPS(1690))酰化脂质 A 结构。人牙龈成纤维细胞(HGFs)作为人牙龈的主要常驻细胞,在调节基质金属蛋白酶(MMPs)方面发挥关键作用,并有助于牙周稳态。本研究旨在探讨牙龈卟啉单胞菌 LPS(1435/1449)和 LPS(1690)以及六酰化大肠杆菌 LPS 刺激下人牙龈成纤维细胞 MMPs1-3 和基质金属蛋白酶组织抑制剂-1(TIMP-1)的表达和调节。通过实时 PCR 和 ELISA 评估 MMPs1-3 和 TIMP-1 的表达。

结果

牙龈卟啉单胞菌 LPS(1690)和大肠杆菌 LPS 处理的细胞中 MMP-3 mRNA 和蛋白表达显著上调,而牙龈卟啉单胞菌 LPS(1435/1449)处理的细胞中未观察到诱导。相反,牙龈卟啉单胞菌 LPS 脂多糖异质性对 MMP-1 和 MMP-2 的表达没有显著影响。牙龈卟啉单胞菌 LPS(1435/1449)和大肠杆菌 LPS 处理的细胞中 TIMP-1 mRNA 表达上调。接下来,通过阻断实验检查了参与牙龈卟啉单胞菌 LPS 诱导 MMP-3 表达的信号转导途径。阻断 p38 MAPK 和 ERK 显著抑制 HGFs 中牙龈卟啉单胞菌 LPS(1690)诱导的 MMP-3 表达。

结论

本研究结果表明,牙龈卟啉单胞菌 LPS 的异质脂多糖结构可调节 HGFs 中 MMP-3 的表达,这可能在牙周病发病机制中起作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e819/3623786/d000508d6507/1471-2180-13-73-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e819/3623786/d58bc9d4e371/1471-2180-13-73-1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e819/3623786/fc8b864498be/1471-2180-13-73-4.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e819/3623786/d000508d6507/1471-2180-13-73-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e819/3623786/d58bc9d4e371/1471-2180-13-73-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e819/3623786/d62380fd536d/1471-2180-13-73-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e819/3623786/e7cf4a0ff161/1471-2180-13-73-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e819/3623786/fc8b864498be/1471-2180-13-73-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e819/3623786/1fd6b5d24c44/1471-2180-13-73-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e819/3623786/d000508d6507/1471-2180-13-73-6.jpg

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