• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

NLRP3 和 AIM2 炎性小体的表达受 LPS 和钛离子调节,增加肺泡骨源性间充质干细胞中活性 IL-1β 的释放。

NLRP3 and AIM2 inflammasomes expression is modified by LPS and titanium ions increasing the release of active IL-1β in alveolar bone-derived MSCs.

机构信息

Department of Oral Surgery and Implant Dentistry, School of Dentistry, University of Granada, 18071 Granada, Spain.

Instituto de Investigación Biosanitaria (IBS) de Granada, 18012 Granada, Spain.

出版信息

Stem Cells Transl Med. 2024 Aug 16;13(8):826-841. doi: 10.1093/stcltm/szae042.

DOI:10.1093/stcltm/szae042
PMID:39013640
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11328940/
Abstract

Periodontitis and peri-implantitis are inflammatory diseases of infectious etiology that lead to the destruction of the supporting tissues located around teeth or implants. Although both pathologies share several characteristics, it is also known that they show important differences which could be due to the release of particles and metal ions from the implant surface. The activation of the inflammasome pathway is one of the main triggers of the inflammatory process. The inflammatory process in patients who suffer periodontitis or peri-implantitis has been mainly studied on cells of the immune system; however, it is also important to consider other cell types with high relevance in the regulation of the inflammatory response. In that context, mesenchymal stromal cells (MSCs) play an essential role in the regulation of inflammation due to their ability to modulate the immune response. This study shows that the induction of NLRP3 and absent in melanoma 2 (AIM2) inflammasome pathways mediated by bacterial components increases the secretion of active IL-1β and the pyroptotic process on human alveolar bone-derived mesenchymal stromal cells (hABSCs). Interestingly, when bacterial components are combined with titanium ions, NLRP3 expression is further increased while AIM2 expression is reduced. Furthermore, decrease of NLRP3 or AIM2 expression in hABSCs partially reverses the negative effect observed on the progression of the inflammatory process as well as on cell survival. In summary, our data suggest that the progression of the inflammatory process in peri-implantitis could be more acute due to the combined action of organic and inorganic components.

摘要

牙周炎和种植体周围炎是由感染引起的炎症性疾病,导致位于牙齿或种植体周围的支持组织破坏。尽管这两种病理具有许多共同特征,但也已知它们表现出重要的差异,这可能是由于种植体表面颗粒和金属离子的释放。炎性小体途径的激活是炎症过程的主要触发因素之一。患有牙周炎或种植体周围炎的患者的炎症过程主要在免疫系统的细胞上进行了研究;然而,考虑到在炎症反应调节中具有高度相关性的其他细胞类型也很重要。在这种情况下,间充质基质细胞(MSCs)由于其调节免疫反应的能力,在炎症调节中发挥着重要作用。这项研究表明,细菌成分介导的 NOD、LRR 和富含亮氨酸重复蛋白 3(NLRP3)和缺失黑色素瘤 2(AIM2)炎性小体途径的诱导增加了人肺泡骨源性间充质基质细胞(hABSCs)中活性白细胞介素-1β(IL-1β)的分泌和细胞焦亡过程。有趣的是,当细菌成分与钛离子结合时,NLRP3 的表达进一步增加,而 AIM2 的表达减少。此外,hABSCs 中 NLRP3 或 AIM2 的表达降低部分逆转了观察到的对炎症过程进展和细胞存活的负面影响。总之,我们的数据表明,由于有机和无机成分的联合作用,种植体周围炎的炎症过程可能更为急性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/34b2c09f0dd6/szae042_fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/93195e5b8da6/szae042_fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/28b72a33fe24/szae042_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/29335094908b/szae042_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/d38168a9ceaa/szae042_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/cde838e52b55/szae042_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/c576e950660f/szae042_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/2832925e4384/szae042_fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/34b2c09f0dd6/szae042_fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/93195e5b8da6/szae042_fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/28b72a33fe24/szae042_fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/29335094908b/szae042_fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/d38168a9ceaa/szae042_fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/cde838e52b55/szae042_fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/c576e950660f/szae042_fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/2832925e4384/szae042_fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/edee/11328940/34b2c09f0dd6/szae042_fig7.jpg

相似文献

1
NLRP3 and AIM2 inflammasomes expression is modified by LPS and titanium ions increasing the release of active IL-1β in alveolar bone-derived MSCs.NLRP3 和 AIM2 炎性小体的表达受 LPS 和钛离子调节,增加肺泡骨源性间充质干细胞中活性 IL-1β 的释放。
Stem Cells Transl Med. 2024 Aug 16;13(8):826-841. doi: 10.1093/stcltm/szae042.
2
Inflammasomes NLRP3 and AIM2 in peri-implantitis: A cross-sectional study.种植体周围炎中炎性小体NLRP3和AIM2:一项横断面研究。
Clin Oral Implants Res. 2023 Dec;34(12):1342-1353. doi: 10.1111/clr.14174. Epub 2023 Aug 29.
3
Analysis of the expression of NLRP3 and AIM2 in periapical lesions with apical periodontitis and microbial analysis outside the apical segment of teeth.分析伴有根尖周炎的根尖周病变和牙尖段外微生物中 NLRP3 和 AIM2 的表达。
Arch Oral Biol. 2017 Jun;78:39-47. doi: 10.1016/j.archoralbio.2017.02.006. Epub 2017 Feb 6.
4
Chronic cerebral hypoperfusion activates AIM2 and NLRP3 inflammasome.慢性脑灌注不足激活 AIM2 和 NLRP3 炎性小体。
Brain Res. 2020 Jun 1;1736:146779. doi: 10.1016/j.brainres.2020.146779. Epub 2020 Mar 18.
5
Carbon monoxide negatively regulates NLRP3 inflammasome activation in macrophages.一氧化碳对巨噬细胞中NLRP3炎性小体的激活起负调节作用。
Am J Physiol Lung Cell Mol Physiol. 2015 May 15;308(10):L1058-67. doi: 10.1152/ajplung.00400.2014. Epub 2015 Mar 13.
6
Cytokine Secretion and Pyroptosis of Thyroid Follicular Cells Mediated by Enhanced NLRP3, NLRP1, NLRC4, and AIM2 Inflammasomes Are Associated With Autoimmune Thyroiditis.增强的NLRP3、NLRP1、NLRC4和AIM2炎性小体介导的甲状腺滤泡细胞细胞因子分泌和焦亡与自身免疫性甲状腺炎相关。
Front Immunol. 2018 Jun 4;9:1197. doi: 10.3389/fimmu.2018.01197. eCollection 2018.
7
Triggers of NLRC4 and AIM2 inflammasomes induce porcine IL-1β secretion.NLRC4和AIM2炎性小体的激活剂可诱导猪白细胞介素-1β的分泌。
Vet Res Commun. 2018 Dec;42(4):265-273. doi: 10.1007/s11259-018-9729-x. Epub 2018 Aug 10.
8
Correlation between Inflammasomes and Microbiota in Peri-Implantitis.种植体周围炎中炎症小体与微生物群的相关性。
Int J Mol Sci. 2024 Jan 12;25(2):961. doi: 10.3390/ijms25020961.
9
The role of NLRP3 and AIM2 in inflammasome activation during Brucella abortus infection.NLRP3和AIM2在布鲁氏菌流产感染期间炎性小体激活中的作用。
Semin Immunopathol. 2017 Feb;39(2):215-223. doi: 10.1007/s00281-016-0581-1. Epub 2016 Jul 12.
10
Enhanced IL-1β Release Following NLRP3 and AIM2 Inflammasome Stimulation Is Linked to mtROS in Airway Macrophages in Pulmonary Fibrosis.NLRP3 和 AIM2 炎性小体刺激后 IL-1β 的释放与肺纤维化气道巨噬细胞中线粒体 ROS 的产生有关。
Front Immunol. 2021 Jun 15;12:661811. doi: 10.3389/fimmu.2021.661811. eCollection 2021.

引用本文的文献

1
Cross-talk between NLRP3 and AIM2 inflammasomes in macrophage activation by LPS and titanium ions.NLRP3与AIM2炎性小体在脂多糖和钛离子激活巨噬细胞过程中的相互作用
Mol Med. 2025 Jun 9;31(1):223. doi: 10.1186/s10020-025-01290-7.
2
AIM2-Driven Inflammation in Periodontitis: Mechanisms and Systemic Implications.AIM2驱动的牙周炎炎症:机制及全身影响
J Inflamm Res. 2025 May 30;18:6983-6997. doi: 10.2147/JIR.S505907. eCollection 2025.
3
Correlation between Inflammasomes and Microbiota in Peri-Implantitis.种植体周围炎中炎症小体与微生物群的相关性。

本文引用的文献

1
Inflammasomes NLRP3 and AIM2 in peri-implantitis: A cross-sectional study.种植体周围炎中炎性小体NLRP3和AIM2:一项横断面研究。
Clin Oral Implants Res. 2023 Dec;34(12):1342-1353. doi: 10.1111/clr.14174. Epub 2023 Aug 29.
2
Modulation of NLRP3 inflammasomes activation contributes to improved survival and function of mesenchymal stromal cell spheroids.调控 NLRP3 炎性小体激活有助于提高间充质基质细胞球体的存活率和功能。
Mol Ther. 2023 Mar 1;31(3):890-908. doi: 10.1016/j.ymthe.2022.12.014. Epub 2022 Dec 24.
3
Impact of Oral Mesenchymal Stem Cells Applications as a Promising Therapeutic Target in the Therapy of Periodontal Disease.
Int J Mol Sci. 2024 Jan 12;25(2):961. doi: 10.3390/ijms25020961.
口腔间充质干细胞应用于牙周病治疗的研究进展
Int J Mol Sci. 2022 Nov 3;23(21):13419. doi: 10.3390/ijms232113419.
4
Ti Ions Induce IL-1β Release by Activation of the NLRP3 Inflammasome in a Human Macrophage Cell Line.钛离子通过激活人巨噬细胞系中的 NLRP3 炎性小体诱导白细胞介素-1β释放。
Inflammation. 2022 Oct;45(5):2027-2037. doi: 10.1007/s10753-022-01672-7. Epub 2022 Jun 21.
5
Interferon activated gene 204 protects against bone loss in experimental periodontitis.干扰素激活基因 204 可预防实验性牙周炎中的骨质流失。
J Periodontol. 2022 Sep;93(9):1366-1377. doi: 10.1002/JPER.21-0668. Epub 2022 Jun 10.
6
NLRP3 Is Involved in Neutrophil Mobilization in Experimental Periodontitis.NLRP3 参与实验性牙周炎中的中性粒细胞动员。
Front Immunol. 2022 Feb 23;13:839929. doi: 10.3389/fimmu.2022.839929. eCollection 2022.
7
Biome-microbiome interactions in peri-implantitis: A pilot investigation.种植体周围炎中的生物-微生物相互作用:一项初步研究。
J Periodontol. 2022 Jun;93(6):814-823. doi: 10.1002/JPER.21-0423. Epub 2022 Apr 9.
8
Specific inhibition of the NLRP3 inflammasome suppresses immune overactivation and alleviates COVID-19 like pathology in mice.特异性抑制 NLRP3 炎性小体可抑制免疫过度激活,并减轻小鼠的类 COVID-19 病理。
EBioMedicine. 2022 Jan;75:103803. doi: 10.1016/j.ebiom.2021.103803. Epub 2021 Dec 31.
9
AIM2 inhibits the proliferation, invasion and migration, and promotes the apoptosis of osteosarcoma cells by inactivating the PI3K/AKT/mTOR signaling pathway.AIM2 通过抑制 PI3K/AKT/mTOR 信号通路抑制骨肉瘤细胞的增殖、侵袭和迁移,促进其凋亡。
Mol Med Rep. 2022 Feb;25(2). doi: 10.3892/mmr.2021.12569. Epub 2021 Dec 16.
10
NLRP3 knockout enhances immune infiltration and inflammatory responses and improves survival in a burn sepsis model.NLRP3 敲除增强免疫浸润和炎症反应,提高烧伤脓毒症模型的生存率。
Immunology. 2022 Feb;165(2):195-205. doi: 10.1111/imm.13427. Epub 2021 Nov 24.