PDF(Pubmed)
Abstract：
UNASSIGNED: The oral cavity and gut tract, being interconnected and rich in microbiota, may have a shared influence on gingivitis. However, the specific role of distinct gut microbiota taxa in gingivitis remains unexplored. Utilizing Mendelian Randomization (MR) as an ideal method for causal inference avoiding reverse causality and potential confounding factors, we conducted a comprehensive two-sample MR study to uncover the potential genetic causal impact of gut microbiota on gingivitis.
UNASSIGNED: Instrumental variables were chosen from single nucleotide polymorphisms (SNPs) strongly associated with 418 gut microbiota taxa, involving 14,306 individuals. Gingivitis, with 4,120 cases and 195,395 controls, served as the outcome. Causal effects were assessed using random-effect inverse variance-weighted, weighted median, and MR-Egger methods. For replication and meta-analysis, gingivitis data from IEU OpenGWAS were employed. Sensitivity analyses included Cochran\'s Q tests, funnel plots, leave-one-out analyses, and MR-Egger intercept tests. This study aimed to assess the genetic correlation between the genetically predicted gut microbiota and gingivitis using linkage disequilibrium score regression (LDSC).
UNASSIGNED: Three gut microbiota taxa (class Actinobacteria id.419, family Defluviitaleaceae id.1924, genus Defluviitaleaceae UCG011 id.11287) are predicted to causally contribute to an increased risk of gingivitis (P< 0.05). Additionally, four gut microbiota taxa (class Actinobacteria id.419, genus Escherichia Shigella id.3504, genus Ruminococcaceae UCG002 id.11360) potentially exhibit inhibitory causal effects on the risk of gingivitis (P< 0.05). No significant evidence of heterogeneity or pleiotropy is detected. Our findings indicate a suggestive genetic correlation between class Actinobacteria id.419, class Bacteroidia id.912, family Defluviitaleaceae id.1924, genus Escherichia Shigella id.3504 and gingivitis.
UNASSIGNED: Our study establishes the genetic causal effect of 418 gut microbiota taxa on gingivitis, offering insights for clinical interventions targeting gingivitis. Subsequent research endeavors are essential to corroborate the findings of our present study.
UNASSIGNED: Instrumental variables were chosen from single nucleotide polymorphisms (SNPs) strongly associated with 418 gut microbiota taxa, involving 14,306 individuals. Gingivitis, with 4,120 cases and 195,395 controls, served as the outcome. Causal effects were assessed using random-effect inverse variance-weighted, weighted median, and MR-Egger methods. For replication and meta-analysis, gingivitis data from IEU OpenGWAS were employed. Sensitivity analyses included Cochran\'s Q tests, funnel plots, leave-one-out analyses, and MR-Egger intercept tests. This study aimed to assess the genetic correlation between the genetically predicted gut microbiota and gingivitis using linkage disequilibrium score regression (LDSC).
UNASSIGNED: Three gut microbiota taxa (class Actinobacteria id.419, family Defluviitaleaceae id.1924, genus Defluviitaleaceae UCG011 id.11287) are predicted to causally contribute to an increased risk of gingivitis (P< 0.05). Additionally, four gut microbiota taxa (class Actinobacteria id.419, genus Escherichia Shigella id.3504, genus Ruminococcaceae UCG002 id.11360) potentially exhibit inhibitory causal effects on the risk of gingivitis (P< 0.05). No significant evidence of heterogeneity or pleiotropy is detected. Our findings indicate a suggestive genetic correlation between class Actinobacteria id.419, class Bacteroidia id.912, family Defluviitaleaceae id.1924, genus Escherichia Shigella id.3504 and gingivitis.
UNASSIGNED: Our study establishes the genetic causal effect of 418 gut microbiota taxa on gingivitis, offering insights for clinical interventions targeting gingivitis. Subsequent research endeavors are essential to corroborate the findings of our present study.
摘要：
■口腔和肠道，相互联系并富含微生物群，可能对牙龈炎有共同的影响。然而,不同的肠道微生物群分类群在牙龈炎中的具体作用仍有待探索。利用孟德尔随机化（MR）作为因果推断的理想方法，避免反向因果关系和潜在的混杂因素，我们进行了一项全面的双样本MR研究,以揭示肠道菌群对牙龈炎的潜在遗传因果影响.
■仪器变量选自与418个肠道微生物群分类群密切相关的单核苷酸多态性(SNPs)。涉及14306人。牙龈炎,有4120例病例和195395例对照，作为结果。因果关系使用随机效应逆方差加权，加权中位数，和MR-Egger方法。对于复制和荟萃分析，采用IEUOpenGWAS的牙龈炎数据。敏感性分析包括科克伦Q检验，漏斗图,遗漏分析，和MR-Egger拦截测试。本研究旨在使用连锁不平衡评分回归（LDSC）评估遗传预测的肠道微生物群与牙龈炎之间的遗传相关性。
■预计三种肠道微生物群分类群（放线菌属id.419，Defluviitaleaceae属id.1924，Defluviitalaceae属UCG011id.11287）会导致牙龈炎的风险增加（P<0.05）。此外,四个肠道微生物群（放线菌属id.419，大肠杆菌志贺氏菌属id.3504，RuminococcaceaeUCG002id.11360）可能对牙龈炎的风险具有抑制作用（P<0.05）。没有检测到异质性或多效性的显著证据。我们的发现表明放线菌id.419类，拟杆菌类id.912类，去氟氏杆菌科id.1924，埃希氏杆菌属id.3504和牙龈炎之间存在暗示性遗传相关性。
■我们的研究建立了418个肠道微生物群分类群对牙龈炎的遗传因果效应，为针对牙龈炎的临床干预提供见解。随后的研究努力对于证实我们本研究的发现至关重要。
■仪器变量选自与418个肠道微生物群分类群密切相关的单核苷酸多态性(SNPs)。涉及14306人。牙龈炎,有4120例病例和195395例对照，作为结果。因果关系使用随机效应逆方差加权，加权中位数，和MR-Egger方法。对于复制和荟萃分析，采用IEUOpenGWAS的牙龈炎数据。敏感性分析包括科克伦Q检验，漏斗图,遗漏分析，和MR-Egger拦截测试。本研究旨在使用连锁不平衡评分回归（LDSC）评估遗传预测的肠道微生物群与牙龈炎之间的遗传相关性。
■预计三种肠道微生物群分类群（放线菌属id.419，Defluviitaleaceae属id.1924，Defluviitalaceae属UCG011id.11287）会导致牙龈炎的风险增加（P<0.05）。此外,四个肠道微生物群（放线菌属id.419，大肠杆菌志贺氏菌属id.3504，RuminococcaceaeUCG002id.11360）可能对牙龈炎的风险具有抑制作用（P<0.05）。没有检测到异质性或多效性的显著证据。我们的发现表明放线菌id.419类，拟杆菌类id.912类，去氟氏杆菌科id.1924，埃希氏杆菌属id.3504和牙龈炎之间存在暗示性遗传相关性。
■我们的研究建立了418个肠道微生物群分类群对牙龈炎的遗传因果效应，为针对牙龈炎的临床干预提供见解。随后的研究努力对于证实我们本研究的发现至关重要。
