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

Plasma Metabolomic and Intestinal Microbial Analyses of Patients With Severe Aplastic Anemia.
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严重再生障碍性贫血患者的血浆代谢组学和肠道微生物分析

DOI:
10.3389/fcell.2021.669887
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发表时间:
2021
影响因子:
5.5
通讯作者:
Shao Z
Shao Z
中科院分区:
生物学2区
文献类型:
--
作者:
Shao Y;Qi W;Zhang X;Ran N;Liu C;Fu R;Shao Z

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再生障碍性贫血是由自身免疫异常引起的骨髓衰竭引起的,但重型再生障碍性贫血(SAA)的发病机制还没有很好的表征。为了鉴定SAA的潜在代谢标志物并进一步阐明SAA的发病机制,我们对SAA患者和健康对照者的血浆样品进行了代谢组学研究并表征了肠道微生物群。SAA患者的肠杆菌目和乳酸杆菌目比健康对照组多,而类杆菌目、梭菌目和丹毒菌目比健康对照组少。在物种水平上,大肠杆菌和其他包括Clostridium citroniae的丰度较高,而Prevotella copri,Roseburia faecis和Ruminococcus bromii的丰度较低。SAA组和健康对照组中8种代谢物的血浆浓度存在显著差异。SAA组中存在较高浓度的香豆酸、L-苯丙氨酸和硫酸盐;而L-谷氨酸γ-半醛、可可碱、3a,7a-二羟基-5b-胆甾烷、γ-δ-二氧代戊酸和(12 Z)-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显示异常。这些差异可能反映了SAA免疫缺陷的分子机制。
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 Escherichia coli and others including Clostridium citroniae were higher, whereas those of Prevotella copri, Roseburia faecis, and Ruminococcus bromii 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.
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