Fusobacterium nucleatum facilitates ulcerative colitis through activating IL-17F signaling to NF-κB via the upregulation of CARD3 expression.,The Journal of Pathology

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Fusobacterium nucleatum facilitates ulcerative colitis through activating IL-17F signaling to NF-κB via the upregulation of CARD3 expression.
The Journal of Pathology ( IF 5.6 ) Pub Date : 2019-12-02 , DOI: 10.1002/path.5358
Yongyu Chen _{1,

2} , Yan Chen _{1,

2} , Pan Cao _{1,

2} , Wenhao Su _{1,

2} , Na Zhan _{1,

3} , Weiguo Dong _{1,

2}

Affiliation

Accumulating evidence links Fusobacterium nucleatum with ulcerative colitis (UC). The mechanism by which F. nucleatum promotes intestinal inflammation in UC remains poorly defined. Here, we first examined the abundance and impact of F. nucleatum on disease activity in UC tissues. Next, we isolated a strain of F. nucleatum from UC tissues and explored whether F. nucleatum aggravates the intestinal inflammatory response in vitro and in vivo. We also examined whether F. nucleatum infection involves the NF-κB or IL-17F signaling pathways. Our data showed that F. nucleatum was enriched in 51.78% of UC tissues and was correlated with the clinical course, clinical activity and refractory behavior of UC (p < 0.05). Furthermore, we demonstrated that F. nucleatum promoted intestinal epithelial damage and the expression of the inflammatory cytokines IL-1β, Il-6, IL-17F and TNF-α. Mechanistically, F. nucleatum targeted caspase activation and recruitment domain 3 (CARD3) through NOD2 to activate the IL-17F/NF-κB pathway in vivo and in vitro. Thus, F. nucleatum orchestrates a molecular network involving CARD3 and IL-17F to control the UC process. Measuring and targeting F. nucleatum and its associated pathways will yield valuable insight into the prevention and treatment of UC. © 2019 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

中文翻译：

核梭状芽胞杆菌通过上调CARD3表达激活IL-17F信号传导至NF-κB，从而促进溃疡性结肠炎。

越来越多的证据将核梭状芽胞杆菌与溃疡性结肠炎（UC）联系起来。核镰刀菌促进UC肠道炎症的机制仍然不清楚。在这里，我们首先检查了F. nucleatum的丰度及其对UC组织疾病活动的影响。接下来，我们从UC组织中分离了一种F. nucleatum菌株，并探讨了F. nucleatum是否会在体内和体外加重肠道炎症反应。我们还检查了核衣原体感染是否涉及NF-κB或IL-17F信号通路。我们的数据显示，核裂殖质富集在UC组织的51.78％中，并且与UC的临床病程，临床活性和难治性行为相关（p <0.05）。此外，我们证明了F. nucleatum促进肠道上皮损伤和炎性细胞因子IL-1β的表达，II-6，IL-17F和TNF-α。从机理上讲，核糖核酸分子通过NOD2靶向caspase激活和募集结构域3（CARD3），以在体内和体外激活IL-17F /NF-κB途径。因此，F。nucleatum编排了涉及CARD3和IL-17F的分子网络，以控制UC过程。测量和靶向F. nucleatum及其相关途径将为UC的预防和治疗提供有价值的见解。©2019英国和爱尔兰病理学会。由John Wiley＆Sons，Ltd.出版核及其相关途径将为UC的预防和治疗提供有价值的见识。©2019英国和爱尔兰病理学会。由John Wiley＆Sons，Ltd.出版核及其相关途径将为UC的预防和治疗提供有价值的见识。©2019英国和爱尔兰病理学会。由John Wiley＆Sons，Ltd.出版

更新日期：2019-12-03

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