微囊素-LR 诱导和加剧小肠炎通过NLRP3炎症酶介导的小鼠中烧亡
Yue Yang1, Pan Gong1, Xiuyan Long1
1Department of Gastroenterology, The Third Xiangya Hospital, Central South University, Changsha 410078, China.
Toxins
|July 28, 2023
概括
微囊素-LR (MC-LR) 通过触发NLRP3炎症酶介导的烧灭,可能诱导炎症性肠病 (IBD). 这种毒素还会使硫酸 (DSS) 诱导的大肠炎在小鼠中恶化.
科学领域:
- 胃肠病学 胃肠病学
- 毒理学 毒理学 毒理学
- 免疫学 免疫学 免疫学
背景情况:
- 炎症性肠病 (IBD) 是一种由环境因素影响的慢性疾病.
- 微囊素-LR (MC-LR),一种毒素,已与肠道损伤和IBD有关.
- 通过MC-LR影响IBD的确切机制仍在调查中.
研究的目的:
- 调查MC-LR对IBD发展及其潜在机制的影响.
- 探索MC-LR在硫酸 (DSS) 诱导的大肠炎中的作用.
- 为了确定MC-LR是否会加剧DSS引起的肠炎症.
主要方法:
- 给小鼠提供了PBS (对照),DSS,MC-LR或DSS和MC-LR的组合.
- 大肠炎的严重程度通过体重减轻,疾病活动指数 (DAI),结肠长度,组织损伤和亡来评估.
- 分析了与烧死相关的蛋白质的表达,特别是那些由NLRP3炎症酶介导的蛋白质.
主要成果:
- 无论是MC-LR还是DSS都诱导了结肠炎,其特征是体重减轻,DAI,组织损伤,细胞亡和促炎细胞因子的增加.
- 联合DSS+MC-LR组表现出比单独使用DSS组更严重的结肠炎.
- MC-LR和DSS增加了NLRP3炎酶介导的烧灭;这种效应在DSS + MC-LR组中得到放大.
结论:
- MC-LR可能会通过NLRP3炎症酶介导的炎热致死诱导结肠炎和潜在的IBD.
- MC-LR可以通过相同的NLRP3炎症酶途径加剧DSS诱导的大肠炎.
- 这项研究为IBD的环境触发因素及其机制提供了新的见解.
更多相关视频
08:24Injections of Lipopolysaccharide into Mice to Mimic Entrance of Microbial-derived Products After Intestinal Barrier Breach
Published on: May 2, 2018
19.6K
06:12Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum
Published on: May 3, 2024
2.0K
相关概念视频
01:20Inflammatory Bowel Disease II: Ulcerative Colitis
Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
01:25Inflammatory Bowel Disease III: Crohn's Disease
Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...