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微生物失生症通过循环二核化物推动STING驱动的自身炎症

Takayuki Shibahara¹, Burcu Temizoz², Shiori Egashira³

¹Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan; Laboratory of Mockup Vaccine, Center for Vaccine and Adjuvant Research, National Institutes of Biomedical Innovation, Health and Nutrition, Ibaraki, Osaka, Japan.

Journal of autoimmunity

|May 7, 2025

概括

失生症通过增加微生物和宿主循环二核酸 (CDN) 来驱动与STING相关的血管病变 (SAVI). 针对CDN或微生物组可能为STING驱动的自身炎症性疾病提供个性化治疗.

科学领域:

免疫学免疫学免疫学
微生物学微生物学
遗传学遗传学是一个

背景情况:

异常刺激干扰素基因 (STING) 路径激活会导致自身炎症性疾病,如在婴儿期发病的与STING相关的血管病变 (SAVI).
将STING激活与SAVI病理联系在一起的机制尚未完全理解.
SAVI涉及系统性炎症,影响血管,皮肤和肺部.

研究的目的:

调查微生物失生症和循环二核酸 (CDN) 在SAVI病变发生中的作用.
探索STING通路参与其他自身免疫性疾病,如全身性红斑狼 (SLE).
确定潜在的生物标志物和STING驱动疾病的治疗点.

主要方法:

研究了具有N153S STING突变的SAVI小鼠,观察了包括大肠炎和腹在内的表型.
分析了小鼠和患者的肠道微生物群组成,并量化了微生物和宿主衍生的CDN.
向SAVI小鼠服用抗生素,以评估对炎症的影响.
在SAVI,SLE和类风湿性关节炎 (RA) 患者中,与疾病生物标志物相关的全身CDN水平.

主要成果:

腹的SAVI小鼠表现出肠道失调,减少了短链脂肪酸生产者和增加了细分丝状细菌.
在腹的SAVI小鼠和SAVI患者中发现了微生物和宿主CDN的升高.
抗生素治疗减少了SAVI小鼠的炎症,证实了失生症的作用.
在SLE患者中,微生物CDN与I型干扰素得分和抗dsDNA抗体相关,与RA不同.

结论:

微生物失生症和循环二核酸 (CDN) 的升高是SAVI中STING激活的关键驱动因素.
系统性CDN作为STING驱动的自身炎症和自身免疫疾病的潜在生物标志物.
针对基于CDN配置文件的cGAS或微生物组,可以提供个性化的治疗策略.

关键词:

自动炎症是一种自发性炎症.循环性二核酸是循环性的二核酸.失生症是一种失生症.微生物组是一个微生物组.萨维尔是什么意思?刺痛是一种刺痛.

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