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在喘和动脉样硬化中,肠肺血管轴沿着微生物群驱动的免疫失调
Elena-Larisa Zimbru1,2, Răzvan-Ionuț Zimbru1,2, Florina-Maria Bojin1,2,3
1Center of Immuno-Physiology and Biotechnologies, Department of Functional Sciences, "Victor Babes" University of Medicine and Pharmacy, 300041 Timisoara, Romania.
Biomedicines
|January 28, 2026
概括
肠道微生物失调症通过肠-肺-血管轴连接喘和动脉样硬化. 分享的微生物和代谢物签名为诊断和治疗这些炎症状况提供了潜力.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 心血管医学 心血管医学
背景情况:
- 喘和动脉样硬化往往并存,共享由肠道微生物失衡影响的免疫代谢途径.
- 肠-肺-血管轴被提议作为理解共享炎症的统一框架.
- 这个轴连接上皮质和内皮质炎症,超越组织特异性疾病界限.
研究的目的:
- 审查喘和动脉样硬化相关的微生物群驱动的途径.
- 识别连接肠道失调与呼吸和心血管功能障碍的微生物种群,代谢物和网络.
- 探索微生物特征和代谢模式的诊断和治疗潜力.
主要方法:
- 一个有针对性的叙事审查临床,实验和多omics研究从过去五年.
- 对研究的系统评估,重点是肠-肺-血管轴和宿主-微生物群相互作用.
- 重点是特定的微生物种群,代谢物 (如SCFA,TMAO,BA,LPS) 和免疫代谢网络.
主要成果:
- 肠道失生症,以减少短链脂肪酸 (SCFA) 和增加病原体为特征,损害了上皮和内皮壁垒.
- 这种失生症促进Th2/Th17炎症和内皮损伤,将肠道健康与呼吸和血管疾病联系起来.
- 关键代谢物如SCFA,三甲基胺N氧化物 (TMAO) 和脂多糖 (LPS) 作为分子介质.
结论:
- 喘和动脉样硬化中共享的微生物和代谢物签名支持肠-肺-血管轴作为一个共同的致病性框架.
- 微生物和代谢学分析可以改善风险分层,并指导向治疗.
- 整合微生物组信息的诊断和个性化干预措施可能会减少系统性炎症和疾病负担.
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