| BMC Microbiology | |
| Porphyromonas gingivalis ATCC 33277 promotes intercellular adhesion molecule-1 expression in endothelial cells and monocyte-endothelial cell adhesion through macrophage migration inhibitory factor | |
| Wanyue Xu1  | |
| [1] Department of Periodontics and Oral Biology, School of Stomatology, China Medical University, Shenyang, China | |
| 关键词: Porphyromonas gingivalis; Macrophage migration inhibitory factor; Intercellular cell adhesion molecule-1; Endothelial cells; | |
| DOI : 10.1186/s12866-018-1156-1 | |
| 学科分类:微生物学和免疫学 | |
| 来源: BioMed Central | |
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【 摘 要 】
Porphyromonas gingivalis (P. gingivalis), one of the main pathogenic bacteria involved in periodontitis, induces the expression of intercellular adhesion molecule − 1 (ICAM-1) and monocyte-endothelial cell adhesion. This effect plays a pivotal role in atherosclerosis development. Macrophage migration inhibitory factor (MIF) is a multifunctional cytokine and critically affects atherosclerosis pathogenesis. In this study, we tested the involvement of MIF in the P. gingivalis ATCC 33277-enhanced adhesive properties of endothelial cells. Endothelial MIF expression was enhanced by P. gingivalis ATCC 33277 infection. The MIF inhibitor ISO-1 inhibited ICAM-1 production in endothelial cells, and monocyte-endothelial cell adhesion was induced by P. gingivalis ATCC 33277 infection. However, the addition of exogenous human recombinant MIF to P. gingivalis ATCC 33277-infected endothelial cells facilitated monocyte recruitment by promoting ICAM-1 expression in endothelial cells. These experiments revealed that MIF in endothelial cells participates in the pro-atherosclerotic lesion formation caused by P. gingivalis ATCC 33277 infection. Our novel findings identify a more detailed pathological role of P. gingivalis ATCC 33277 in atherosclerosis.
【 授权许可】
CC BY
【 预 览 】
| Files | Size | Format | View |
|---|---|---|---|
| RO201910251940668ZK.pdf | 1823KB |
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