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重型再生障碍性贫血患者的血浆代谢组学和肠道微生物分析

Plasma Metabolomic and Intestinal Microbial Analyses of Patients With Severe Aplastic Anemia.

作者信息

Shao Yuanyuan, Qi Weiwei, Zhang Xiaomei, Ran Ningyuan, Liu Chunyan, Fu Rong, Shao Zonghong

机构信息

Department of Hematology, General Hospital of Tianjin Medical University, Tianjin, China.

出版信息

Front Cell Dev Biol. 2021 Aug 23;9:669887. doi: 10.3389/fcell.2021.669887. eCollection 2021.

Abstract

Aplastic anemia results from bone marrow failure caused by an autoimmune abnormality, but the pathogenesis of severe aplastic anemia (SAA) is not well characterized. To identify potential metabolic markers of SAA and to further elucidate the pathogenetic mechanisms of SAA, we performed a metabolomic study of plasma samples and characterized the intestinal microbiota of patients with SAA and healthy controls. Patients with SAA had more Enterobacteriales and Lactobacillales, but fewer Bacteroidales, Clostridiales, and Erysipelotrichales than healthy controls. At the species level, the abundances of and others including were higher, whereas those of , , and were lower. Eight metabolites showed significantly different plasma concentrations in the SAA and healthy control groups. Coumaric acid, L-phenylalanine, and sulfate were present at higher concentrations in the SAA group; whereas L-glutamic γ-semialdehyde, theobromine, 3a, 7a-dihydroxy-5b-cholestane, γ-δ-dioxovaleric acid, and (12Z)-9, 10-dihydroxyoctadec-12-enoic acid were present at lower concentrations. In conclusion, patients with SAA show abnormalities in both their plasma metabolomes and intestinal microbial compositions. These differences might reflect the molecular mechanisms involved in the defective immunity that characterizes SAA.

摘要

再生障碍性贫血是由自身免疫异常导致的骨髓衰竭引起的,但严重再生障碍性贫血(SAA)的发病机制尚未完全明确。为了确定SAA的潜在代谢标志物并进一步阐明SAA的发病机制,我们对血浆样本进行了代谢组学研究,并对SAA患者和健康对照者的肠道微生物群进行了特征分析。与健康对照者相比,SAA患者的肠杆菌目和乳杆菌目更多,但拟杆菌目、梭菌目和丹毒丝菌目更少。在物种水平上,[具体物种1]和其他包括[具体物种2]在内的物种丰度较高,而[具体物种3]、[具体物种4]和[具体物种5]的丰度较低。8种代谢物在SAA组和健康对照组中的血浆浓度存在显著差异。香豆酸、L-苯丙氨酸和硫酸盐在SAA组中的浓度较高;而L-谷氨酸γ-半醛、可可碱、3a,7a-二羟基-5b-胆甾烷、γ-δ-二氧戊酸和(12Z)-9,10-二羟基十八碳-12-烯酸的浓度较低。总之,SAA患者的血浆代谢组和肠道微生物组成均存在异常。这些差异可能反映了SAA特征性免疫缺陷所涉及的分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9149/8419359/94961499505e/fcell-09-669887-g001.jpg

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