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-  2018 

粪肠球菌LTA通过促进ROS的高表达活化NLRP3炎性体
Enterococcus Faecalis LTA Activates NLRP3 Inflammasome by Promoting High Expression of ROS

DOI: 10.13701/j.cnki.kqyxyj.2018.02.002

Keywords: NLRP3炎性体,粪肠球菌,LTA,ROS,
NLRP3 inflammasome
, Enterococcus faecalis, LTA, ROS

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Abstract:

摘要 目的:检测粪肠球菌脂磷壁酸LTA能否通过激活活性氧而活化NLRP3炎性体。方法:粪肠球菌LTA作用于小鼠巨噬细胞RAW264.7,运用Western blot、ELISA及 Real-time qPCR法检测NLRP3炎性体蛋白及mRNA的表达。还原型烟酰胺腺嘌呤二核苷酸磷酸酶氧化酶抑制剂DPI抑制活性氧(reactive oxygen species,ROS)的产生,荧光染色及流式细胞仪检测ROS的表达。结果:LTA作用于RAW264.7细胞24小时后,NLRP3、Caspase-1、IL-1β蛋白及mRNA的表达量均明显高于阴性对照组(P<0.05)。DPI可有效抑制ROS的产生,ROS表达被抑制后,NLRP3炎性体蛋白及mRNA的表达亦明显降低。结论:LTA是粪肠球菌活化NLRP3炎性体的毒力因子,主要借助于ROS的产生

References

[1]  Wang L,Dong M,Song Q, et al. Relationship of biofilm formation and gelE gene expression in Enterococcus faecalis recovered from root canals in patients requiring endodontic retreatment[J]. J Endod, 2011, 37(5)∶631-636
[2]  Han SH, Kim JH, Seo HS, et al. Lipoteichoic acid-induced nitric oxide production depends on the activation of platelet-activating factor receptor and Jak2[J]. J Immunol, 2006,176(1)∶573-579
[3]  Provenzano JC, Antunes HS, Alves FR, et al. Host-bacterial interactions in post-treatment pical periodontitis: a metaproteome analysis[J]. J Endod, 2016, 42(6)∶880-885
[4]  Tian YG, Zhang XL, Zhang K, et al. Effect of enterococcus faecalis lipoteichoic acid on apoptosis in human osteoblast-like cells[J]. J Endod, 2013, 39(5)∶632-637
[5]  刘生波,刘元元.NLRP3在大鼠实验性根尖周炎中的表达[J].口腔医学研究,2013,29(11)∶1002-1004
[6]  Wang L, Jin H, Ye D, et al. Enterococcus faecalis lipoteichoic acid-induced NLRP3 inflammasome via the ctivation of the nuclear factor kappa B pathway[J]. J Endod, 2016, 42(7)∶1093-1100.
[7]  Franchi L, Mu oz-Planillo R, N ez G. Sensing and reacting to microbesthrough the inflammasomes[J]. Nat Immunol, 2012, 13(4)∶325 332
[8]  Wen H, Gris D, Lei Y, Jha S, et al. Fatty acidinduced NLRP3-ASC inflammasome activation interferes with insulin signaling[J]. Nat Immunol, 2011, 12(5)∶408 415
[9]  Dai L, DeFee MR, Cao Y, et al. Lipoteichoic acid (LTA) and lipopolysaccharides (LPS) from periodontal pathogenic bacteria facilitate oncogenic herpesvirus infection within primary oral cells[J]. PLoS One, 2014, 9(6)∶1-11
[10]  Ferrari PH,Cai S,Bombana AC. Effect of endodontic procedures on enterococc enteric bacteria and yeasts in primary endodontic infections[J]. IntEndod J, 2005, 38(6)∶372-380
[11]  Zhao L, Chen J, Cheng L,et al. Effects of Enterococcus faecalislipoteichoic acid on receptor activator of nuclear factor-κB ligand and osteoprotegerin expression in periodontal ligament fibroblasts[J]. IntEndod J, 2014, 47(2)∶163-172
[12]  王娇娇,王丽娜,叶丹丹,等.NLRP3/Caspase-1炎性体通路在大鼠根尖周炎中表达的研究[J].口腔医学研究,2016,32(6)∶549-553
[13]  Koizumi Y, Toma C, Higa N, Nohara T, et al. Inflammasome activation via intracellular NLRs triggered by bacterial infection[J]. Cell Microbiol, 2012, 14(2)∶149 154
[14]  Bedard K, Krause KH. The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology[J]. Physiol Rev, 2007, 87(1)∶245-313
[15]  Traore K, Zirkin B, Thimmulappa RK, et al. Upregulation of TLR1, TLR2, TLR4, and IRAK-2 expression during ML-1 cell differentiation to macrophages: role in the potentiation of cellular responses to LPS and LTA[J]. ISRN Oncol, 2012(10)∶641246

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