Soluble CD14 Enhances the Response of Periodontal Ligament Stem Cells to P. gingivalis Lipopolysaccharide

被引:41
作者
Andrukhov, Oleh [1 ]
Andrukhova, Olena [2 ]
Ozdemir, Burcu [1 ,3 ]
Haririan, Hady [1 ]
Mueller-Kern, Michael [1 ]
Moritz, Andreas [1 ]
Rausch-Fan, Xiaohui [1 ]
机构
[1] Med Univ Vienna, Univ Clin Dent, Div Conservat Dent & Periodontol, Vienna, Austria
[2] Univ Vet Med, Dept Biomed Sci, Vienna, Austria
[3] Gazi Univ, Fac Dent, Dept Periodontol, Ankara, Turkey
关键词
MESENCHYMAL STROMAL CELLS; PORPHYROMONAS-GINGIVALIS; RECEPTOR; 4; LPS; SCD14; DIFFERENTIATION; INTERLEUKIN-6; ACTIVATION; CHEMOKINES; EXPRESSION;
D O I
10.1371/journal.pone.0160848
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];
摘要
Periodontal ligament stem cells (PDLSCs) are lacking membrane CD14, which is an important component of lipopolysaccharide (LPS) signaling through toll-like receptor (TLR) 4. In the present study we investigated the effect of soluble CD14 on the response of human PDLSCs to LPS of Porphyromonas (P.) gingivalis. Human PDLSCs (hPDLSCs) were stimulated with P. gingivalis LPS in the presence or in the absence of soluble CD14 (sCD14) and the production of interleukin (IL)-6, chemokine C-X-C motif ligand 8 (CXCL8), and chemokine C-C motif ligand 2 (CCL2) was measured. The response to P. gingivalis LPS was compared with that to TLR4 agonist Escherichia coli LPS and TLR2-agonist Pam3CSK4. The response of hPDLSCs to both P. gingivalis LPS and E. coli LPS was significantly enhanced by sCD14. In the absence of sCD14, no significant difference in the hPDLSCs response to two kinds of LPS was observed. These responses were significantly lower compared to that to Pam3CSK4. In the presence of sCD14, the response of hPdLSCs to P. gingivalis LPS was markedly higher than that to E. coli LPS and comparable with that to Pam3CSK4. The response of hPdLSCs to bacterial LPS is strongly augmented by sCD14. Local levels of sCD14 could be an important factor for modulation of the host response against periodontal pathogens.
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页数:13
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