Fusobacterium nucleatumis a Gram-negative anaerobe that occupies a central ecological niche in oral biofilms but has emerged as a trans-compartmental pathogen implicated in gastrointestinal and cardiovascular diseases. In inflammatory bowel diseases,Fusobacterium nucleatumadheres to the intestinal epithelium via adhesins such as FadA, disrupts tight junctions, and induces Toll-like receptor–mediated inflammatory cascades, amplifying epithelial permeability and sustaining mucosal inflammation. In colorectal cancer,Fusobacterium nucleatumpromotes carcinogenesis through multiple mechanisms, including β-catenin activation, modulation of oncogenic microRNAs, and immune evasion via Fap2–TIGIT signaling, while also fostering a pro-inflammatory and immunosuppressive tumor microenvironment. Its enrichment correlates with advanced tumor stage, chemoresistance, and poor prognosis, underscoring its potential as a biomarker and therapeutic target. Beyond the gut,Fusobacterium nucleatumhas been detected in atherosclerotic plaques and endocardial tissues, where it contributes to endothelial dysfunction, foam cell formation, oxidative stress, and plaque instability, thereby linking chronic oral infection with cardiovascular risk. Collectively, evidence suggests thatFusobacterium nucleatumacts as a pathophysiological connector across IBD, CRC, and CVD through conserved mechanisms of adhesion, immune modulation, and inflammation. Understanding these processes provides opportunities for innovative interventions, ranging from targeted antimicrobials and host-directed therapies to dietary and microbiome-based strategies, aimed at mitigating the systemic burden of this organism and improving clinical outcomes across multiple diseases.
具核梭杆菌是一种革兰阴性厌氧菌，在口腔生物膜中占据核心生态位，但已逐渐成为跨腔室传播的病原体，与胃肠道及心血管疾病密切相关。在炎症性肠病中，具核梭杆菌通过FadA等黏附素附着于肠上皮细胞，破坏紧密连接结构，并诱导Toll样受体介导的炎症级联反应，从而加剧上皮通透性并维持黏膜炎症状态。在结直肠癌中，该菌通过β-连环蛋白激活、致癌性微小RNA调控以及Fap2–TIGIT信号通路介导的免疫逃逸等多重机制促进肿瘤发生，同时营造促炎性与免疫抑制的肿瘤微环境。其富集程度与肿瘤晚期分期、化疗耐药及不良预后显著相关，凸显其作为生物标志物和治疗靶点的潜力。在肠道之外，具核梭杆菌已在动脉粥样硬化斑块和心内膜组织中被检出，通过促进内皮功能障碍、泡沫细胞形成、氧化应激及斑块不稳定性，将慢性口腔感染与心血管风险联系起来。总体证据表明，具核梭杆菌通过保守的黏附、免疫调节及炎症机制，成为连接炎症性肠病、结直肠癌与心血管疾病的病理生理纽带。深入理解这些机制为创新干预策略提供了契机，包括靶向抗菌治疗、宿主导向疗法以及基于饮食与微生物组的调控策略，有望减轻该菌引发的全身性病理负担，并改善多种疾病的临床预后。
肿瘤(癌症)患者之家