口腔共生菌和致病菌对人树突状细胞的影响。

T Chino, D M Santer, D Giordano, C Chen, C Li, C-H Chen, R P Darveau, E A Clark
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引用次数: 17

摘要

背景/目的:口腔是一个多样而复杂的微生物群落。细菌在坚硬和柔软的口腔组织中聚集在无根生物膜中,并与宿主进行复杂的细胞对话,这通常将细菌限制在共生和谐的状态。作为慢性炎症反应的一部分,树突状细胞(dc)可能平衡对共生微生物的耐受性和主动免疫。虽然DC在维持肠道内稳态中的作用已被广泛研究,但对于DC对口腔细菌的反应却知之甚少。方法:在这项研究中,我们用致病性和共生革兰氏阳性或革兰氏阴性口腔细菌的细胞壁提取物脉冲人单核细胞来源的未成熟dc (iDCs)。结果:虽然所有细菌提取物都能诱导dc成熟并产生细胞因子/趋化因子,包括白细胞介素-12p40、肿瘤坏死因子- α和单核细胞趋化蛋白-1 (MCP-1),但口腔细菌编程dc的最重要因素是它们是革兰氏阳性还是革兰氏阴性,而不是它们是共生的还是致病的。一般来说,除了牙周病性牙龈卟啉单胞菌外,革兰氏阴性口腔细菌刺激DC成熟和细胞因子产生的浓度低于革兰氏阳性口腔细菌。刺激趋化因子产生所需的细菌阈值比诱导细胞因子所需的阈值低100到1000倍。此外,极低剂量的口腔共生菌可触发单核细胞向dc来源的MCP-1迁移。结论:口腔共生菌与致病菌对dc的编程方式没有质的差异。口腔共生菌诱导的dc源性MCP-1可能通过吸引单核细胞来维持口腔组织的完整性,至少在一定程度上起作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of oral commensal and pathogenic bacteria on human dendritic cells.

Background/aims: The oral cavity harbors a diverse and complex microbial community. Bacteria accumulate on both the hard and soft oral tissues in sessile biofilms and engage the host in an intricate cellular dialog, which normally constrains the bacteria to a state of commensal harmony. Dendritic cells (DCs) are likely to balance tolerance and active immunity to commensal microorganisms as part of chronic inflammatory responses. While the role played by DCs in maintaining intestinal homeostasis has been investigated extensively, relatively little is known about DC responses to oral bacteria.

Methods: In this study, we pulsed human monocyte-derived immature DCs (iDCs) with cell wall extracts from pathogenic and commensal gram-positive or gram-negative oral bacteria.

Results: Although all bacterial extracts tested induced iDCs to mature and produce cytokines/chemokines including interleukin-12p40, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 (MCP-1), the most important factor for programming DCs by oral bacteria was whether they were gram-positive or gram-negative, not whether they were commensal or pathogenic. In general, gram-negative oral bacteria, except for periodontopathic Porphyromonas gingivalis, stimulated DC maturation and cytokine production at lower concentrations than gram-positive oral bacteria. The threshold of bacteria needed to stimulate chemokine production was 100-fold to 1000-fold lower than that needed to induce cytokines. In addition, very low doses of oral commensal bacteria triggered monocytes to migrate toward DC-derived MCP-1.

Conclusion: Oral commensal and pathogenic bacteria do not differ qualitatively in how they program DCs. DC-derived MCP-1 induced in response to oral commensal bacteria may play a role, at least in part, in the maintenance of oral tissue integrity by attracting monocytes.

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