相关实验视频

Updated: Jun 10, 2025

Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis

Analyzing Beneficial Effects of Nutritional Supplements on Intestinal Epithelial Barrier Functions During Experimental Colitis

Published on: January 5, 2017

中性细胞细胞外陷通过cGAS-STING通路诱导DSS诱导的性结肠炎的屏障功能障碍

Tao Sun¹, Ping Wang¹, Xinru Zhai¹

¹School of Life Science and Technology, China Pharmaceutical University, Nanjing, China.

International immunopharmacology

|October 10, 2024

概括

中性细胞外细胞陷 (NETs) 通过激活cGAS-STING通路,使性结肠炎 (UC) 恶化. 阻断这种途径,涉及基氨酸脱敏酶4 (PAD4),可能提供新的UC治疗方法.

科学领域:

免疫学免疫学免疫学
胃肠病学胃肠病学
分子生物学分子生物学

背景情况:

中性粒细胞外细胞陷 (NETs),由基氨酸脱胺酶4 (PAD4) 介导,涉及到性结肠炎 (UC) 病变发生.
干扰素基因 (STING) 途径的循环GMP-AMP合成酶 (cGAS) 刺激器是关键的细胞内DNA传感器,参与炎症.

研究的目的:

研究NETs在UC相关的肠炎和屏障功能障碍中的作用.
为了阐明cGAS-STING路径在NET介导的UC中的参与.

主要方法:

在UC小鼠结肠中评估了STING表达.
使用PAD4基因淘汰阻止NET形成.
在MC38细胞中检查了cGAS-STING通路的NET激活.
评估了STING缺乏对结肠炎严重程度和肠道屏障功能的影响.

主要成果:

在UC小鼠结肠中,STING表达显著升高,在PAD4淘汰后水平降低.
NETs以剂量和时间依赖的方式激活了cGAS-STING通路,诱导炎症性细胞因子分泌和屏障功能障碍.
STING 缺乏改善了临床大肠炎,肠道炎症和屏障缺陷.

结论:

通过NETs激活cGAS-STING通路,并导致UC的肠道炎症和屏障功能障碍.
向cGAS-STING通路为性结肠炎提供了一个潜在的治疗策略.

关键词:

肠道炎症是一种肠道炎症.中性粒细胞外细胞陷乙氨基氨酸减小酶4 性结肠炎是一种在cGAS-STING路径中.

更多相关视频

Systematic Scoring Analysis for Intestinal Inflammation in a Murine Dextran Sodium Sulfate-Induced Colitis Model

Systematic Scoring Analysis for Intestinal Inflammation in a Murine Dextran Sodium Sulfate-Induced Colitis Model

Published on: February 14, 2021

Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy

Visualization of Neutrophil Extracellular Traps in Mesenteric Venules After Mesenteric Ischemia-Reperfusion Injury via Intravital Microscopy

Published on: September 27, 2024

相关概念视频

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI) tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.