多杀性巴氏杆菌毒素通过nod样受体蛋白3炎性体加重结扎诱导的牙周骨丢失和炎症

IF 2.6 2区 生物学 Q3 CELL BIOLOGY
Yineng Han, P. Gao, Qiaolin Yang, Yiping Huang, L. Jia, Yunfei Zheng, Weiran Li
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引用次数: 0

摘要

据报道,nod样受体家族pyrin结构域- 3 (NLRP3)炎症小体参与牙周发病。多杀性巴氏杆菌毒素(PMT)是多杀性巴氏杆菌属非口服革兰氏阴性兼性杆状菌(GNFR)的主要毒力因子。GNFR及其毒素的存在可加重牙周炎。因此,揭示PMT在牙周炎中的调节机制具有重要意义。然而,NLRP3炎性体和PMT在牙周炎中的作用尚不清楚。免疫组化染色和定量逆转录聚合酶链反应(qRT-PCR)结果显示,牙周炎小鼠NLRP3表达升高。通过16S rRNA测序,Nlrp3-/-小鼠牙周骨丢失较少,多杀性巴氏杆菌丰度较低。PMT通过激活B细胞核因子κB轻链增强子(NF-κB)通路,激活NLRP3炎性体,促进NLRP3表达。这种作用被NLRP3抑制剂MCC950逆转。此外,PMT加重了WT小鼠的牙周骨质流失和炎症,而MCC950则减轻了牙周骨质流失和炎症。局部注射PMT的Nlrp3-/-牙周炎模型与PMT治疗后的WT牙周炎小鼠相比,骨质流失和炎症反应较少。综上所述,我们的研究结果表明,PMT通过促进NLRP3表达和激活NLRP3炎性体,加重牙周对结膜的反应,提示NLRP3可能是治疗GNFR引起的牙周炎的有效靶点,MCC950可能是治疗该疾病的潜在药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pasteurella multocida Toxin Aggravates Ligatured-Induced Periodontal Bone Loss and Inflammation via NOD-Like Receptor Protein 3 Inflammasome
NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is reportedly involved in periodontal pathogenesis. Pasteurella multocida toxin (PMT) is the major virulence factor of Pasteurella multocida strains, which belongs to the nonoral gram-negative facultative rods (GNFR). The existence of GNFR and their toxin may aggravate periodontitis. Therefore, it is important to unclose the regulatory mechanisms of PMT in periodontitis. However, the involvement of NLRP3 inflammasome and PMT in periodontitis remain unclear. The results showed that NLRP3 expression was increased in periodontitis mice by immunohistochemical staining and quantitative reverse transcription polymerase chain reaction (qRT-PCR). Nlrp3-/- mice showed less periodontal bone loss and lower abundances of Pasteurella multocida by 16S rRNA sequencing. PMT promoted NLRP3 expressions by activating nuclear factor kappa light chain enhancer of B cells (NF-κB) pathway and activated NLRP3 inflammasome. This effect was reversed by NLRP3 inhibitor MCC950. Furthermore, PMT aggravated periodontal bone loss and inflammation in WT mice, while MCC950 attenuated periodontal bone loss and inflammation. The Nlrp3-/- periodontitis models with PMT local injection showed less bone loss and inflammation compared with WT periodontitis mice after PMT treatment. Taken together, our results showed that PMT aggravates periodontal response to the ligature by promoting NLRP3 expression and activating NLRP3 inflammasome, suggesting that NLRP3 may be an effective target for the treatment of periodontitis caused by GNFR and MCC950 may be a potential drug against this disease.
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来源期刊
Cellular Microbiology
Cellular Microbiology 生物-微生物学
CiteScore
9.70
自引率
0.00%
发文量
26
审稿时长
3 months
期刊介绍: Cellular Microbiology aims to publish outstanding contributions to the understanding of interactions between microbes, prokaryotes and eukaryotes, and their host in the context of pathogenic or mutualistic relationships, including co-infections and microbiota. We welcome studies on single cells, animals and plants, and encourage the use of model hosts and organoid cultures. Submission on cell and molecular biological aspects of microbes, such as their intracellular organization or the establishment and maintenance of their architecture in relation to virulence and pathogenicity are also encouraged. Contributions must provide mechanistic insights supported by quantitative data obtained through imaging, cellular, biochemical, structural or genetic approaches.
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