缺氧环境下LPS诱导人牙周膜成纤维细胞炎性损伤的研究进展
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摘要
内毒素(Lipopolysaccharide,LPS)是牙周炎炎症免疫反应中重要的毒力因子之一,直接或间接地作用于牙周膜成纤维细胞导致其炎性损伤。而牙周膜成纤维细胞因其所处位置的特殊性,长期处于相对缺氧的环境中。所以通过体外模拟牙周膜成纤维细胞发生炎性损伤时的体内环境,有利于阐明缺氧条件下细胞炎性损伤机制。本文就缺氧环境下LPS诱导的人牙周膜成纤维细胞炎性损伤的研究做一系统性回顾。
Lipopolysaccharide( LPS),which is one of the main virulence factors of periodontitis,results in the inflammatory injury of human periodontal ligament cells( h PDLCs) directly or indirectly. However,h PDLCs reside in a inflamed and hypoxic microenvironment due to their special location. Thus,simulating the inflammatory microenvironment of h PDLCs in vivo will be beneficial to clarifying the mechanism of periodontitis. In this paper,research on the inflammatory injury in h PDLCs induced by LPS under hypoxia will be entensively reviewed.
Lipopolysaccharide( LPS),which is one of the main virulence factors of periodontitis,results in the inflammatory injury of human periodontal ligament cells( h PDLCs) directly or indirectly. However,h PDLCs reside in a inflamed and hypoxic microenvironment due to their special location. Thus,simulating the inflammatory microenvironment of h PDLCs in vivo will be beneficial to clarifying the mechanism of periodontitis. In this paper,research on the inflammatory injury in h PDLCs induced by LPS under hypoxia will be entensively reviewed.
引文
[1]Tanaka M,Hanioka T,Takaya K,et al.Association of oxygen tension in human periodontal pockets with gingival inflammation[J].J Periodontol,1998,69(10):1127-1130.
[2]Loginova NK,Krylova OV.Effect of masticatory load on oxygen tension in periodontal tissues[J].Stomatologiia(Mosk),2001,80(1):23-25.
[3]Niklas A,Proff P,Gosau M,et al.The role of hypoxia in orthodontic tooth movement[J].Int J Dent,2013,2013:841840.
[4]Hanioka T,Tanaka M,Takaya K,et al.Pocket oxygen tension in smokers and non-smokers with periodontal disease[J].J Periodontol,2000,71(4):550-554.
[5]Collin HL,Sorsa T,Meurman JH,et al.Salivary matrix metalloproteinase(MMP-8)levels and gelatinase(MMP-9)activities in patients with type 2 diabetes mellitus[J].J Periodontal Res,2000,35(5):259-265.
[6]Mettraux GR,Gusberti FA,Graf H.Oxygen tension(p O2)in untreated human periodontal pockets[J].J Periodontol,1984,55(9):516-521.
[7]Salvi GE,Brown CE,Fujihashi K,et al.Inflammatory mediators of the terminal dentition in adult and early onset periodontitis[J].J Periodontal Res,1998,33(4):212-225.
[8]Yamamoto T,Kita M,Oseko F,et al.Cytokine production in human periodontal ligament cells stimulated with Porphyromonas gingivalis[J].J Periodontal Res,2006,41(6):554-559.
[9]Kato H,Taguchi Y,Tominaga K,et al.Porphyromonas gingivalis LPS inhibits osteoblastic differentiation and promotes pro-inflammatory cytokine production in human periodontal ligament stem cells[J].Arch Oral Biol,2014,59(2):167-175.
[10]王岚,夏佳佳,刘琪,等.脂多糖对人牙周膜干细胞增殖及炎性因子表达的影响[J].华西口腔医学杂志,2013,31(3):286-290.
[11]Park Y,Kim Y,Jung Y,et al.Porphyromonas gingivalis lipopolysaccharide regulates interleukin(IL)-17 and IL-23 expression via SIRT1 modulation in human periodontal ligament cells[J].Cytokine,2012,60(1):284-293.
[12]Moon JS,Cheong NR,Yang SY,et al.Lipopolysaccharideinduced indoleamine 2,3-dioxygenase expression in the periodontal ligament[J].J Periodontal Res,2013,48(6):733-739.
[13]徐婧秋,吴丽萍.脂多糖和白细胞介素-1β对人牙周膜细胞中诱导型一氧化氮合酶表达的影响[J].华西口腔医学杂志,2011,29(4):415-419.
[14]Zhang Y,Li X.Lipopolysaccharide-regulated production of bone sialoprotein and interleukin-8 in human periodontal ligament fibroblasts:the role of toll-like receptors 2 and 4 and the MAPK pathway[J].J Periodontal Res,2015,50(2):141-151.
[15]于鑫,王月秋,李明恒,等.Toll样受体2和4在脂多糖诱导人牙周膜成纤维细胞表达细胞核因子-κB受体活化因子配基中的作用[J].华西口腔医学杂志,2012,30(3):325-328.
[16]Seo T,Cha S,Kim T,et al.Porphyromonas gingivalis-derived lipopolysaccharide-mediated activation of MAPK signaling regulates inflammatory response and differentiation in human periodontal ligament fibroblasts[J].J Microbiol(Seoul,Korea),2012,50(2):311-319.
[17]Zhang Q,Wang C,Liu Z,et al.Notch signal suppresses Toll-like receptor-triggered inflammatory responses in macrophages by inhibiting extracellular signal-regulated kinase 1/2-mediated nuclear factor kappa B activation[J].J Biol Chem,2012,287(9):6208-6217.
[18]Du A,Zhao S,Wan L,et al.MicroRNA expression profile of human periodontal ligament cells under the influence of Porphyromonas gingivalis LPS[J].J Cell Mol Med,2016,20(7):1329-1338.
[19]宋忠臣,束蓉,李希庭,等.氯化钴化学模拟低氧对牙周膜成纤维细胞增殖及凋亡的影响[J].上海口腔医学,2009,18(5):489-492.
[20]宋爱梅,侯超,陈家芳,等.缺氧对人牙周膜成纤维细胞基质金属蛋白酶和组织金属蛋白酶抑制物mRNA表达的影响[J].中华口腔医学杂志,2012,47(10):599-604.
[21]Ng K,Li J,Ng KM,et al.Expression of hypoxia-inducible factor-1alpha in human periodontal tissue[J].J Periodontal Res,2011,82(1):136-141.
[22]Park H,Baek K H,Lee H,et al.Hypoxia inducible factor-1alpha directly induces the expression of receptor activator of nuclear factor-kappa B ligand in periodontal ligament fibroblasts[J].Mol Cells,2011,31(6):573-578.
[23]Majmundar AJ,Wong WJ,Simon MC.Hypoxia-inducible factors and the response to hypoxic stress[J].Mol Cells,2010,40(2):294-309.
[24]Jiang BH,Rue E,Wang GL,et al.Dimerization,DNA binding,and transactivation properties of hypoxia-inducible factor 1[J].J Biol Chem 1996,271(30):17771-17778.
[25]Huang M,Paglialunga S,Wong JM,et al.Role of prolyl hydroxylase domain proteins in the regulation of insulin secretion[J].Physiological reports,2016,4(5):e12722.
[26]Watanabe T,Yasue A,Tanaka E.Inhibition of transforming growth factor beta1/Smad3 signaling decreases hypoxia-inducible factor-1alpha protein stability by inducing prolyl hydroxylase 2 expression in human periodontal ligament cells[J].J Biol Chem,2013,84(9):1346-1352.
[27]Jian C,Li C,Ren Y,et al.Hypoxia augments lipopolysaccharideinduced cytokine expression in periodontal ligament cells[J].Inflammation,2014,37(5):1413-1423.
[28]Pumklin J,Bhalang K,Pavasant P.Hypoxia enhances the effect of lipopolysaccharide-stimulated IL-1beta expression in human periodontal ligament cells[J].Odontology,2016,104(3):338-346.
[29]Golz L,Memmert S,Rath-Deschner B,et al.LPS from P.gingivalis and hypoxia increases oxidative stress in periodontal ligament fibroblasts and contributes to periodontitis[J].Mediators Inflamm,2014,2014:986264.
[30]Golz L,Memmert S,Rath-Deschner B,et al.Hypoxia and P.gingivalis synergistically induce HIF-1 and NF-kappa B activation in PDL cells and periodontal diseases[J].Mediators Inflamm,2015,2015:438085.
[31]Vasconcelos RC,Costa A DLL,Freitas RDA,et al.Immunoexpression of HIF-1alpha and VEGF in periodontal disease and healthy gingival tissues[J].Braz Dent J,2016,27(2):117-122.
[32]Memmert S,Golz L,Putz P,et al.Regulation of p53 under hypoxic and inflammatory conditions in periodontium[J].Clin Oral Investig,2015,20(7):1781-1789.
[33]Kim Y,Shin S,Kang K,et al.Nicotine and lipopolysaccharide stimulate the production of MMPs and prostaglandin E2 by hypoxia-inducible factor-1alpha up-regulation in human periodontal ligament cells[J].J Periodontal Res,2012,47(6):719-728.
[34]Bae W,Shin M,Kang S,et al.HIF-2 inhibition supresses inflammatory responses and osteoclastic differentiation in human periodontal ligament cells[J].J Cell Biochem,2015,116(7):1241-1255.
[35]Moon J,Lee J,Lee J.Subgingival microbiome in smokers and non-smokers in korean chronic periodontitis patients[J].Mol Oral Microbiol,2015,30(3):227-241.
[36]Salminen A,Kopra KAE,Hyvarinen K,et al.Quantitative PCR analysis of salivary pathogen burden in periodontitis[J].Front Cell Infect Microbiol,2015,5:69.
[2]Loginova NK,Krylova OV.Effect of masticatory load on oxygen tension in periodontal tissues[J].Stomatologiia(Mosk),2001,80(1):23-25.
[3]Niklas A,Proff P,Gosau M,et al.The role of hypoxia in orthodontic tooth movement[J].Int J Dent,2013,2013:841840.
[4]Hanioka T,Tanaka M,Takaya K,et al.Pocket oxygen tension in smokers and non-smokers with periodontal disease[J].J Periodontol,2000,71(4):550-554.
[5]Collin HL,Sorsa T,Meurman JH,et al.Salivary matrix metalloproteinase(MMP-8)levels and gelatinase(MMP-9)activities in patients with type 2 diabetes mellitus[J].J Periodontal Res,2000,35(5):259-265.
[6]Mettraux GR,Gusberti FA,Graf H.Oxygen tension(p O2)in untreated human periodontal pockets[J].J Periodontol,1984,55(9):516-521.
[7]Salvi GE,Brown CE,Fujihashi K,et al.Inflammatory mediators of the terminal dentition in adult and early onset periodontitis[J].J Periodontal Res,1998,33(4):212-225.
[8]Yamamoto T,Kita M,Oseko F,et al.Cytokine production in human periodontal ligament cells stimulated with Porphyromonas gingivalis[J].J Periodontal Res,2006,41(6):554-559.
[9]Kato H,Taguchi Y,Tominaga K,et al.Porphyromonas gingivalis LPS inhibits osteoblastic differentiation and promotes pro-inflammatory cytokine production in human periodontal ligament stem cells[J].Arch Oral Biol,2014,59(2):167-175.
[10]王岚,夏佳佳,刘琪,等.脂多糖对人牙周膜干细胞增殖及炎性因子表达的影响[J].华西口腔医学杂志,2013,31(3):286-290.
[11]Park Y,Kim Y,Jung Y,et al.Porphyromonas gingivalis lipopolysaccharide regulates interleukin(IL)-17 and IL-23 expression via SIRT1 modulation in human periodontal ligament cells[J].Cytokine,2012,60(1):284-293.
[12]Moon JS,Cheong NR,Yang SY,et al.Lipopolysaccharideinduced indoleamine 2,3-dioxygenase expression in the periodontal ligament[J].J Periodontal Res,2013,48(6):733-739.
[13]徐婧秋,吴丽萍.脂多糖和白细胞介素-1β对人牙周膜细胞中诱导型一氧化氮合酶表达的影响[J].华西口腔医学杂志,2011,29(4):415-419.
[14]Zhang Y,Li X.Lipopolysaccharide-regulated production of bone sialoprotein and interleukin-8 in human periodontal ligament fibroblasts:the role of toll-like receptors 2 and 4 and the MAPK pathway[J].J Periodontal Res,2015,50(2):141-151.
[15]于鑫,王月秋,李明恒,等.Toll样受体2和4在脂多糖诱导人牙周膜成纤维细胞表达细胞核因子-κB受体活化因子配基中的作用[J].华西口腔医学杂志,2012,30(3):325-328.
[16]Seo T,Cha S,Kim T,et al.Porphyromonas gingivalis-derived lipopolysaccharide-mediated activation of MAPK signaling regulates inflammatory response and differentiation in human periodontal ligament fibroblasts[J].J Microbiol(Seoul,Korea),2012,50(2):311-319.
[17]Zhang Q,Wang C,Liu Z,et al.Notch signal suppresses Toll-like receptor-triggered inflammatory responses in macrophages by inhibiting extracellular signal-regulated kinase 1/2-mediated nuclear factor kappa B activation[J].J Biol Chem,2012,287(9):6208-6217.
[18]Du A,Zhao S,Wan L,et al.MicroRNA expression profile of human periodontal ligament cells under the influence of Porphyromonas gingivalis LPS[J].J Cell Mol Med,2016,20(7):1329-1338.
[19]宋忠臣,束蓉,李希庭,等.氯化钴化学模拟低氧对牙周膜成纤维细胞增殖及凋亡的影响[J].上海口腔医学,2009,18(5):489-492.
[20]宋爱梅,侯超,陈家芳,等.缺氧对人牙周膜成纤维细胞基质金属蛋白酶和组织金属蛋白酶抑制物mRNA表达的影响[J].中华口腔医学杂志,2012,47(10):599-604.
[21]Ng K,Li J,Ng KM,et al.Expression of hypoxia-inducible factor-1alpha in human periodontal tissue[J].J Periodontal Res,2011,82(1):136-141.
[22]Park H,Baek K H,Lee H,et al.Hypoxia inducible factor-1alpha directly induces the expression of receptor activator of nuclear factor-kappa B ligand in periodontal ligament fibroblasts[J].Mol Cells,2011,31(6):573-578.
[23]Majmundar AJ,Wong WJ,Simon MC.Hypoxia-inducible factors and the response to hypoxic stress[J].Mol Cells,2010,40(2):294-309.
[24]Jiang BH,Rue E,Wang GL,et al.Dimerization,DNA binding,and transactivation properties of hypoxia-inducible factor 1[J].J Biol Chem 1996,271(30):17771-17778.
[25]Huang M,Paglialunga S,Wong JM,et al.Role of prolyl hydroxylase domain proteins in the regulation of insulin secretion[J].Physiological reports,2016,4(5):e12722.
[26]Watanabe T,Yasue A,Tanaka E.Inhibition of transforming growth factor beta1/Smad3 signaling decreases hypoxia-inducible factor-1alpha protein stability by inducing prolyl hydroxylase 2 expression in human periodontal ligament cells[J].J Biol Chem,2013,84(9):1346-1352.
[27]Jian C,Li C,Ren Y,et al.Hypoxia augments lipopolysaccharideinduced cytokine expression in periodontal ligament cells[J].Inflammation,2014,37(5):1413-1423.
[28]Pumklin J,Bhalang K,Pavasant P.Hypoxia enhances the effect of lipopolysaccharide-stimulated IL-1beta expression in human periodontal ligament cells[J].Odontology,2016,104(3):338-346.
[29]Golz L,Memmert S,Rath-Deschner B,et al.LPS from P.gingivalis and hypoxia increases oxidative stress in periodontal ligament fibroblasts and contributes to periodontitis[J].Mediators Inflamm,2014,2014:986264.
[30]Golz L,Memmert S,Rath-Deschner B,et al.Hypoxia and P.gingivalis synergistically induce HIF-1 and NF-kappa B activation in PDL cells and periodontal diseases[J].Mediators Inflamm,2015,2015:438085.
[31]Vasconcelos RC,Costa A DLL,Freitas RDA,et al.Immunoexpression of HIF-1alpha and VEGF in periodontal disease and healthy gingival tissues[J].Braz Dent J,2016,27(2):117-122.
[32]Memmert S,Golz L,Putz P,et al.Regulation of p53 under hypoxic and inflammatory conditions in periodontium[J].Clin Oral Investig,2015,20(7):1781-1789.
[33]Kim Y,Shin S,Kang K,et al.Nicotine and lipopolysaccharide stimulate the production of MMPs and prostaglandin E2 by hypoxia-inducible factor-1alpha up-regulation in human periodontal ligament cells[J].J Periodontal Res,2012,47(6):719-728.
[34]Bae W,Shin M,Kang S,et al.HIF-2 inhibition supresses inflammatory responses and osteoclastic differentiation in human periodontal ligament cells[J].J Cell Biochem,2015,116(7):1241-1255.
[35]Moon J,Lee J,Lee J.Subgingival microbiome in smokers and non-smokers in korean chronic periodontitis patients[J].Mol Oral Microbiol,2015,30(3):227-241.
[36]Salminen A,Kopra KAE,Hyvarinen K,et al.Quantitative PCR analysis of salivary pathogen burden in periodontitis[J].Front Cell Infect Microbiol,2015,5:69.