PT -期刊文章盟Yi-Heng王盟郑征燕盟-斯丹罗盟Jing-Juan胡锦涛AU -吴美盟金赵盟Wei-Feng刘盟- Cai李盟Ke-Xuan刘TI -琥珀酸肠道microbiota-derived加剧急性肺损伤小鼠肠缺血/再灌注后援助- 10.1183/13993003.00840 -2022 DP - 2023年2月01 TA -欧洲呼吸杂志PG - 2200840 VI - 61 IP - 2 4099 - //www.qdcxjkg.com/content/61/2/2200840.short 4100 - //www.qdcxjkg.com/content/61/2/2200840.full所以欧元和J2023 2月01;61 AB -介绍急性肺损伤(ALI)是一种发病率和死亡率的主要原因后,肠道缺血/再灌注(I / R)。肠道微生物群及其代谢副产品作为gut-lung轴的重要调节器。本研究旨在定义琥珀酸的作用,一个关键微生物群代谢物,在肠I / R-induced阿里进展。方法小鼠的肠道微生物群和肺受到肠I / R使用16 s rRNA基因测序分析。琥珀酸水平变化测定无菌鼠或传统的老鼠使用抗生素治疗。Succinate-induced肺泡巨噬细胞分化及其对肺泡上皮细胞凋亡的影响进行评估在琥珀酸受体1 (Sucnr1)缺乏在小鼠肺泡巨噬细胞转染小鼠和Sucnr1-short干扰RNA。琥珀酸含量测定的患者接受心肺旁路,包括肠I / R。结果琥珀酸积累在肺肠I / R,这与一个不平衡的succinate-producing succinate-consuming肠道里的细菌,但不是肺。琥珀酸积累在无菌鼠缺席,被肠道微生物群的损耗用抗生素逆转,表明肠道微生物群是肺琥珀酸的来源。此外,琥珀酸促进肺泡巨噬细胞分化,肺泡上皮细胞凋亡和肺损伤肠I / R。 Conversely, knockdown of Sucnr1 or blockage of SUCNR1 in vitro and in vivo reversed the effects of succinate by modulating the phosphoinositide 3-kinase-AKT/hypoxia-inducible factor-1α pathway. Plasma succinate levels significantly correlated with intestinal I/R-related lung injury after cardiopulmonary bypass.Conclusion Gut microbiota-derived succinate exacerbates intestinal I/R-induced ALI through SUCNR1-dependent alveolar macrophage polarisation, identifying succinate as a novel target for gut-derived ALI in critically ill patients.Succinate accumulation in the lungs is associated with the imbalance of succinate-producing and -consuming bacteria in the gut during intestinal ischaemia/reperfusion. Lung injury was exacerbated by succinate via alveolar macrophage polarisation. https://bit.ly/3fTR9AM