IR@PKUHSC  > 北京大学口腔医学院  > 牙周科
学科主题口腔医学
Porphyromonas gingivalis Exacerbates Ligature-Induced, RANKL-Dependent Alveolar Bone Resorption via Differential Regulation of Toll-Like Receptor 2 (TLR2) and TLR4
Lin, Jiang1,2; Bi, Liangjia2; Yu, Xiaoqian1,3; Kawai, Toshihisa1; Taubman, Martin A.1; Shen, Baozhong4; Han, Xiaozhe1
刊名INFECTION AND IMMUNITY
2014-10-01
DOI10.1128/IAI.02084-14
82期:10页:4127-4134
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Immunology ; Infectious Diseases
研究领域[WOS]Immunology ; Infectious Diseases
关键词[WOS]NF-KAPPA-B ; PERIODONTAL-DISEASE ; IL-10 PRODUCTION ; HEMAGGLUTININ B ; DENDRITIC CELLS ; INNATE IMMUNITY ; HOST RESPONSE ; PATHOGEN ; LIPOPOLYSACCHARIDE ; RECOGNITION
英文摘要

Toll-like receptors (TLRs) play a key role in the innate immune responses to periodontal pathogens in periodontal disease. The present study was performed to determine the roles of TLR2 and TLR4 signaling in alveolar bone resorption, using a Porphyromonas gingivalis-associated ligature-induced periodontitis model in mice. Wild-type (WT), Tlr2(-/-), and Tlr4(-/-) mice (8 to 10 weeks old) in the C57/BL6 background were used. Silk ligatures were applied to the maxillary second molars in the presence or absence of live P. gingivalis infection. Ligatures were removed from the second molars on day 14, and mice were kept for another 2 weeks before sacrifice for final analysis (day 28). On day 14, there were no differences in alveolar bone resorption and gingival RANKL expression between mice treated with ligation plus P. gingivalis infection and mice treated with ligation alone. Gingival interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF-alpha) expression was increased, whereas IL-10 expression was decreased in WT and Tlr2(-/-) mice but not in Tlr4(-/-) mice. On day 28, WT and Tlr4(-/-) mice treated with ligation plus P. gingivalis infection showed significantly increased bone loss and gingival RANKL expression compared to those treated with ligation alone, whereas such an increase was diminished in Tlr2(-/-) mice. Gingival TNF-alpha upregulation and IL-10 downregulation were observed only in WT and Tlr4(-/-) mice, not in Tlr2(-/-) mice. In all mice, bone resorption induced by ligation plus P. gingivalis infection was antagonized by local anti-RANKL antibody administration. This study suggests that P. gingivalis exacerbates ligature- induced, RANKL-dependent periodontal bone resorption via differential regulation of TLR2 and TLR4 signaling.

语种英语
WOS记录号WOS:000341935100013
项目编号DE-003420 ; DE-021837
资助机构NIH from the National Institute of Dental and Craniofacial Research
引用统计
被引频次:26[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/62702
专题北京大学口腔医学院_牙周科
作者单位1.Forsyth Inst, Dept Immunol & Infect Dis, Cambridge, MA USA
2.Harbin Med Univ, Hosp 4, Dept Stomatol, Harbin, Peoples R China
3.Peking Univ, Sch & Hosp Stomatol, Dept Periodontol, Beijing 100871, Peoples R China
4.Harbin Med Univ, Dept Radiol, Hosp 4, Harbin, Peoples R China
推荐引用方式
GB/T 7714
Lin, Jiang,Bi, Liangjia,Yu, Xiaoqian,et al. Porphyromonas gingivalis Exacerbates Ligature-Induced, RANKL-Dependent Alveolar Bone Resorption via Differential Regulation of Toll-Like Receptor 2 (TLR2) and TLR4[J]. INFECTION AND IMMUNITY,2014,82(10):4127-4134.
APA Lin, Jiang.,Bi, Liangjia.,Yu, Xiaoqian.,Kawai, Toshihisa.,Taubman, Martin A..,...&Han, Xiaozhe.(2014).Porphyromonas gingivalis Exacerbates Ligature-Induced, RANKL-Dependent Alveolar Bone Resorption via Differential Regulation of Toll-Like Receptor 2 (TLR2) and TLR4.INFECTION AND IMMUNITY,82(10),4127-4134.
MLA Lin, Jiang,et al."Porphyromonas gingivalis Exacerbates Ligature-Induced, RANKL-Dependent Alveolar Bone Resorption via Differential Regulation of Toll-Like Receptor 2 (TLR2) and TLR4".INFECTION AND IMMUNITY 82.10(2014):4127-4134.
条目包含的文件
条目无相关文件。
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Lin, Jiang]的文章
[Bi, Liangjia]的文章
[Yu, Xiaoqian]的文章
百度学术
百度学术中相似的文章
[Lin, Jiang]的文章
[Bi, Liangjia]的文章
[Yu, Xiaoqian]的文章
必应学术
必应学术中相似的文章
[Lin, Jiang]的文章
[Bi, Liangjia]的文章
[Yu, Xiaoqian]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。