Tobacco smoke exacerbates Filifactor alocis pathogenicity.
Tobacco smoke exacerbates Filifactor alocis pathogenicity.
复制标题
烟草烟雾加剧 Filifactor alocis 的致病性。
DOI：
10.1111/jcpe.13729
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发表时间：
2023
影响因子：
6.7
通讯作者：
Scott,DavidA
中科院分区：
文献类型：
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作者：
Iskander,MinaMZ;Lamont,GwynethJ;Tan,Jinlian;Pisano,Michele;Uriarte,SilviaM;Scott,DavidA
目的Filifactoralocishas最近成为一种牙周病菌，似乎在吸烟者的口腔中茁壮成长。我们假设识别烟雾反应性F. alocisgenes将提供深入了解适应性策略和香烟烟雾会增强。材料与方法F. alocis在体外生长，并通过RNAseq确定香烟烟雾提取物响应基因。将小鼠暴露于或不暴露于主流1 R6 F研究香烟烟雾并感染F。alocis，或没有，在牙周炎的急性结扎模型。关键的临床，感染和免疫数据收集。alocisgrowth不受烟雾调节的影响，只有少数基因受到烟雾暴露的特异性调节。小鼠体重减少、食蟹猴识别抗体产生的差异、免疫特征改变以及牙槽骨丢失改变都可归因于烟雾暴露和/或F。结论F. alocisis很好地适应烟草丰富的条件，其发病机制是由烟草烟雾暴露增强。吸烟暴露的牙周炎结扎模型显示出作为一种工具的希望，可以进一步揭示烟草增强的细菌诱导疾病的机制。
AimFilifactor alocishas recently emerged as a periodontal pathobiont that appears to thrive in the oral cavity of smokers. We hypothesized that identification of smoke‐responsiveF. alocisgenes would provide insight into adaptive strategies and that cigarette smoke would enhanceF. alocispathogenesis in vivo.Materials and MethodsF. alociswas grown in vitro and cigarette smoke extract‐responsive genes determined by RNAseq. Mice were exposed, or not, to mainstream 1R6F research cigarette smoke and infected withF. alocis, or not, in an acute ligature model of periodontitis. Key clinical, infectious, and immune data were collected.ResultsIn culture,F. alocisgrowth was unaffected by smoke conditioning and only a small number of genes were specifically regulated by smoke exposure. Reduced murine mass, differences inF. alocis‐cognizant antibody production, and altered immune profiles as well as altered alveolar bone loss were all attributable to smoke exposure and/orF. alocisinfection in vivo.ConclusionsF. alocisis well‐adapted to tobacco‐rich conditions and its pathogenesis is enhanced by tobacco smoke exposure. A smoke‐exposed ligature model of periodontitis shows promise as a tool with which to further unravel mechanisms underlying tobacco‐enhanced, bacteria‐induced disease.