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评估暴露于牙周病原体的牙龈成纤维细胞的细胞因子释放情况。

assessment of cytokine release from gingival fibroblasts exposed to periodontal pathogens.

作者信息

Tripathi Kaushal Pati, Mishra Rohit, Choubey Varsha, Kumar Ajay, Aglawe Arohi, Gulati Anshul

机构信息

Department of Periodontics & Implantology, Hitkarini Dental College & Hospital, Jabalpur 482005, Madhya Pradesh, India.

Department of Oral Medicine & Radiology, Faculty of Dental Sciences, Institute of Medical Sciences, Banaras Hindu University, Varanasi-221005, Uttar Pradesh, India.

出版信息

Bioinformation. 2025 Jun 30;21(6):1501-1505. doi: 10.6026/973206300211501. eCollection 2025.

DOI:10.6026/973206300211501
PMID:40978615
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12449547/
Abstract

Cytokine responses of gingival fibroblasts from healthy and inflamed tissues upon exposure to (LPS) are of interest. Samples were obtained from 20 individuals undergoing periodontal procedures. Inflamed fibroblasts showed elevated secretion of IL-6, MCP-1, IL-8, and GRO. LPS induced a stronger cytokine response than controls. Thus, inflamed fibroblasts can mount a secondary inflammatory response to periodontal pathogens.

摘要

来自健康和发炎组织的牙龈成纤维细胞在暴露于脂多糖（LPS）时的细胞因子反应备受关注。样本取自20名接受牙周治疗的个体。发炎的成纤维细胞显示出白细胞介素-6（IL-6）、单核细胞趋化蛋白-1（MCP-1）、白细胞介素-8（IL-8）和生长调节致癌基因α（GRO）分泌增加。脂多糖诱导的细胞因子反应比对照组更强。因此，发炎的成纤维细胞可对牙周病原体产生继发性炎症反应。

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本文引用的文献

1
Compromised inflammatory cytokine response to P. gingivalis LPS by fibroblasts from inflamed human gingiva.炎症性人牙龈成纤维细胞对 P. gingivalis LPS 的炎症细胞因子反应受损。
Clin Oral Investig. 2018 Mar;22(2):919-927. doi: 10.1007/s00784-017-2171-6. Epub 2017 Jul 8.
2
Differential cytokine patterns in mouse macrophages and gingival fibroblasts after stimulation with porphyromonas gingivalis or Escherichia coli lipopolysaccharide.牙龈卟啉单胞菌或大肠杆菌脂多糖刺激后小鼠巨噬细胞和牙龈成纤维细胞中细胞因子的差异模式。
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Variable cell responses to P. gingivalis lipopolysaccharide.细胞对牙龈卟啉单胞菌脂多糖的反应各异。
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Porphyromonas gingivalis culture supernatants differentially regulate interleukin-1beta and interleukin-18 in human monocytic cells.牙龈卟啉单胞菌培养上清液对人单核细胞中白细胞介素-1β和白细胞介素-18有不同的调节作用。
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Porphyromonas gingivalis lipopolysaccharide induces tumor necrosis factor-alpha and interleukin-6 secretion, and CCL25 gene expression, in mouse primary gingival cell lines: interleukin-6-driven activation of CCL2.牙龈卟啉单胞菌脂多糖可诱导小鼠原代牙龈细胞系分泌肿瘤坏死因子-α和白细胞介素-6，并促进CCL25基因表达：白细胞介素-6驱动CCL2激活。
J Periodontal Res. 2008 Aug;43(4):431-9. doi: 10.1111/j.1600-0765.2008.01090.x.
6
Mapping the pathogenesis of periodontitis: a new look.剖析牙周炎的发病机制：新视角
J Periodontol. 2008 Aug;79(8 Suppl):1560-8. doi: 10.1902/jop.2008.080213.
7
Differential interactions of fimbriae and lipopolysaccharide from Porphyromonas gingivalis with the Toll-like receptor 2-centred pattern recognition apparatus.牙龈卟啉单胞菌菌毛和脂多糖与以Toll样受体2为中心的模式识别装置的差异相互作用
Cell Microbiol. 2006 Oct;8(10):1557-70. doi: 10.1111/j.1462-5822.2006.00730.x.
8
Cytokine profiling of macrophages exposed to Porphyromonas gingivalis, its lipopolysaccharide, or its FimA protein.暴露于牙龈卟啉单胞菌、其脂多糖或其菌毛蛋白A的巨噬细胞的细胞因子分析。
Infect Immun. 2005 Feb;73(2):935-43. doi: 10.1128/IAI.73.2.935-943.2005.
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Periodontol 2000. 2004;34:9-21. doi: 10.1046/j.0906-6713.2002.003421.x.
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Porphyromonas gingivalis lipopolysaccharide signaling in gingival fibroblasts-CD14 and Toll-like receptors.牙龈卟啉单胞菌脂多糖在牙龈成纤维细胞中的信号传导——CD14和Toll样受体
Crit Rev Oral Biol Med. 2002;13(2):132-42. doi: 10.1177/154411130201300204.