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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.

Stem Cells Transl Med. 2024-8-16

[2]
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Clin Oral Implants Res. 2023-12

[3]
Analysis of the expression of NLRP3 and AIM2 in periapical lesions with apical periodontitis and microbial analysis outside the apical segment of teeth.

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[4]
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[5]
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[6]
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[7]
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[8]
Correlation between Inflammasomes and Microbiota in Peri-Implantitis.

Int J Mol Sci. 2024-1-12

[9]
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[10]
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引用本文的文献

[1]
Cross-talk between NLRP3 and AIM2 inflammasomes in macrophage activation by LPS and titanium ions.

Mol Med. 2025-6-9

[2]
AIM2-Driven Inflammation in Periodontitis: Mechanisms and Systemic Implications.

J Inflamm Res. 2025-5-30

[3]
Correlation between Inflammasomes and Microbiota in Peri-Implantitis.

Int J Mol Sci. 2024-1-12

本文引用的文献

[1]
Inflammasomes NLRP3 and AIM2 in peri-implantitis: A cross-sectional study.

Clin Oral Implants Res. 2023-12

[2]
Modulation of NLRP3 inflammasomes activation contributes to improved survival and function of mesenchymal stromal cell spheroids.

Mol Ther. 2023-3-1

[3]
Impact of Oral Mesenchymal Stem Cells Applications as a Promising Therapeutic Target in the Therapy of Periodontal Disease.

Int J Mol Sci. 2022-11-3

[4]
Ti Ions Induce IL-1β Release by Activation of the NLRP3 Inflammasome in a Human Macrophage Cell Line.

Inflammation. 2022-10

[5]
Interferon activated gene 204 protects against bone loss in experimental periodontitis.

J Periodontol. 2022-9

[6]
NLRP3 Is Involved in Neutrophil Mobilization in Experimental Periodontitis.

Front Immunol. 2022

[7]
Biome-microbiome interactions in peri-implantitis: A pilot investigation.

J Periodontol. 2022-6

[8]
Specific inhibition of the NLRP3 inflammasome suppresses immune overactivation and alleviates COVID-19 like pathology in mice.

EBioMedicine. 2022-1

[9]
AIM2 inhibits the proliferation, invasion and migration, and promotes the apoptosis of osteosarcoma cells by inactivating the PI3K/AKT/mTOR signaling pathway.

Mol Med Rep. 2022-2

[10]
NLRP3 knockout enhances immune infiltration and inflammatory responses and improves survival in a burn sepsis model.

Immunology. 2022-2

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