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首页> 美国卫生研究院文献>NPJ Biofilms and Microbiomes >The making of a miscreant: tobacco smoke and the creation of pathogen-rich biofilms
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The making of a miscreant: tobacco smoke and the creation of pathogen-rich biofilms

机译：制造恶性物质：烟草烟雾和富含病原体的生物膜的形成

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We have previously reported that oral biofilms in clinically healthy smokers are pathogen-rich, and that this enrichment occurs within 24 h of biofilm formation. The present investigation aimed to identify a mechanism by which smoking creates this altered community structure. By combining in vitro microbial–mucosal interface models of commensal (consisting of Streptococcus oralis, Streptococcus sanguis, Streptococcus mitis, Actinomyces naeslundii, Neisseria mucosa and Veillonella parvula) and pathogen-rich (comprising S.oralis, S.sanguis, S.mitis, A.naeslundii, N.mucosa and V.parvula, Fusobacterium nucleatum, Porphyromonas gingivalis, Filifactor alocis, Dialister pneumosintes, Selenonomas sputigena, Selenominas noxia, Catonella morbi, Parvimonas micra and Tannerella forsythia) communities with metatranscriptomics, targeted proteomics and fluorescent microscopy, we demonstrate that smoke exposure significantly downregulates essential metabolic functions within commensal biofilms, while significantly increasing expression of virulence genes, notably lipopolysaccharide (LPS), flagella and capsule synthesis. By contrast, in pathogen-rich biofilms several metabolic pathways were over-expressed in response to smoke exposure. Under smoke-rich conditions, epithelial cells mounted an early and amplified pro-inflammatory and oxidative stress response to these virulence-enhanced commensal biofilms, and a muted early response to pathogen-rich biofilms. Commensal biofilms also demonstrated early and widespread cell death. Similar results were observed when smoke-free epithelial cells were challenged with smoke-conditioned biofilms, but not vice versa. In conclusion, our data suggest that smoke-induced transcriptional shifts in commensal biofilms triggers a florid pro-inflammatory response, leading to early commensal death, which may preclude niche saturation by these beneficial organisms. The cytokine-rich, pro-oxidant, anaerobic environment sustains inflammophilic bacteria, and, in the absence of commensal antagonism, may promote the creation of pathogen-rich biofilms in smokers.
机译：我们以前曾报道过，临床上健康的吸烟者的口腔生物膜富含病原体，并且这种富集发生在生物膜形成后24小时之内。本研究旨在确定吸烟导致这种社区结构改变的机制。通过结合共生的体外微生物-粘膜界面模型（由链球菌，血链球菌，米氏链球菌，内生放线菌，粘膜奈瑟氏球菌和小菜蛾组成）和病原体丰富（包括S.oralis，S.sanguis，S.mitis） naeslundii，粘膜N.parvula和V.parvula，核梭状芽胞杆菌，牙龈卟啉单胞菌，Alocis肺炎，Dialister肺炎，Slenonomas sputigena，Selenominas noxia，Catonella morbi，Parvimonas cracra和Tannerella forsythics以及带有偏meta的原发性微藻，粘液菌证明吸烟暴露会显着下调共生生物膜内的基本代谢功能，同时显着增加毒力基因的表达，尤其是脂多糖（LPS），鞭毛和胶囊的合成。相比之下，在富含病原体的生物膜中，响应于烟暴露，一些代谢途径被过度表达。在浓烟条件下，上皮细胞对这些增强了毒力的共生生物膜具有早期和放大的促炎和氧化应激反应，而对富含病原体生物膜的早期响应却无声。共生生物膜还显示出早期和广泛的细胞死亡。用无烟生物膜挑战无烟上皮细胞时，观察到相似的结果，反之亦然。总之，我们的数据表明，烟雾诱导的共生生物膜转录转变触发了短暂的促炎症反应，导致共生早期死亡，这可能阻止了这些有益生物的生态位饱和。富含细胞因子，促氧化剂的厌氧环境维持了嗜热细菌，并且在缺乏共生拮抗作用的情况下，可能促进吸烟者体内富含致病菌生物膜的形成。

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