Fusobacterium nucleatum dysregulates inflammatory cytokines and NLRP3 inflammasomes in oral cells.

IF 2.9 3区医学 Q1 DENTISTRY, ORAL SURGERY & MEDICINE

Oral diseases Pub Date : 2024-10-01 Epub Date: 2024-02-26 DOI:10.1111/odi.14899

Jingzhuo Sun, Susu Feng, Tian Ding, Ting Wang, Lingqian Du, Wenyan Kang, Shaohua Ge

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引用次数: 0

Abstract

Objective: This study aimed to clarify the difference in Fusobacterium nucleatum (F. nucleatum) induced inflammatory cytokines and nod-like receptor protein 3 (NLRP3) inflammasomes dysregulation among three periodontal cells.

Methods: Oral epithelial cells (HIOECs), THP-1 macrophages, and human gingival fibroblasts (HGFs) were exposed to F. nucleatum with/without adenosine triphosphate (ATP) and nigericin (Nig). Cell morphology was assessed by scanning electron microscopy. qRT-PCR, protein microarrays, and bioinformatic methods were used to evaluate the cytokines and their complex interplay. NLRP3 inflammasomes activation was detected by western blotting and ELISA.

Results: F. nucleatum adhered to and invaded cells. In HIOECs, F. nucleatum enhanced interleukin (IL)-1α/1β/6/10/13, TNF-α, and interferon (IFN)-γ expression. In THP-1 macrophages, F. nucleatum up-regulated IL-1α/1β/6/10 and TNF-α levels. In HGFs, F. nucleatum increased IL-6 levels. F. nucleatum and ATP synergistically boosted IFN-γ level in THP-1 macrophages and IL-13 level in HGFs. IL-1α/1β/6, and TNF-α served as epicenters of the inflammatory response. Additionally, F. nucleatum activated NLRP3 inflammasomes in HIOECs, and ATP/Nig boosted the activation. F. nucleatum also triggered NLRP3 inflammasomes in THP-1 macrophages, but in HGFs, only NLRP3 and caspase-1 levels were elevated.

Conclusion: F. nucleatum infiltrated periodontal supporting cells and dysregulated inflammatory cytokines and NLRP3 inflammasomes.

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核分枝杆菌对口腔细胞中的炎症细胞因子和 NLRP3 炎症小体调节失调。

研究目的本研究旨在阐明三种牙周细胞中核分枝杆菌（F. nucleatum）诱导的炎性细胞因子和类结核受体蛋白 3（NLRP3）炎性体调节紊乱的差异：方法：将口腔上皮细胞（HIOECs）、THP-1 巨噬细胞和人牙龈成纤维细胞（HGFs）暴露于含有/不含三磷酸腺苷（ATP）和尼革菌素（Nig）的核酸噬菌体中。采用 qRT-PCR、蛋白芯片和生物信息学方法评估细胞因子及其复杂的相互作用。通过免疫印迹和酶联免疫吸附检测 NLRP3 炎性体的激活情况：结果：F. nucleatum粘附并侵入细胞。在 HIOECs 中，F. nucleatum 增强了白细胞介素（IL）-1α/1β/6/10/13、TNF-α 和干扰素（IFN）-γ 的表达。在 THP-1 巨噬细胞中，F. nucleatum 上调 IL-1α/1β/6/10 和 TNF-α 的水平。在成纤维细胞中，F. nucleatum 增加了 IL-6 的水平。F. nucleatum 和 ATP 可协同提高 THP-1 巨噬细胞中的 IFN-γ 水平和 HGFs 中的 IL-13 水平。IL-1α/1β/6 和 TNF-α 是炎症反应的中心。此外，F. nucleatum激活了HIOECs中的NLRP3炎性体，而ATP/Nig促进了这种激活。F. nucleatum还触发了THP-1巨噬细胞中的NLRP3炎性体，但在HGFs中，只有NLRP3和caspase-1水平升高：结论：F. nucleatum浸润牙周支持细胞，导致炎性细胞因子和 NLRP3 炎性体失调。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Oral diseases 医学-牙科与口腔外科

CiteScore

7.60

自引率

5.30%

发文量

325

审稿时长

4-8 weeks

期刊介绍： Oral Diseases is a multidisciplinary and international journal with a focus on head and neck disorders, edited by leaders in the field, Professor Giovanni Lodi (Editor-in-Chief, Milan, Italy), Professor Stefano Petti (Deputy Editor, Rome, Italy) and Associate Professor Gulshan Sunavala-Dossabhoy (Deputy Editor, Shreveport, LA, USA). The journal is pre-eminent in oral medicine. Oral Diseases specifically strives to link often-isolated areas of dentistry and medicine through broad-based scholarship that includes well-designed and controlled clinical research, analytical epidemiology, and the translation of basic science in pre-clinical studies. The journal typically publishes articles relevant to many related medical specialties including especially dermatology, gastroenterology, hematology, immunology, infectious diseases, neuropsychiatry, oncology and otolaryngology. The essential requirement is that all submitted research is hypothesis-driven, with significant positive and negative results both welcomed. Equal publication emphasis is placed on etiology, pathogenesis, diagnosis, prevention and treatment.