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HIV 感染精英控制者的肠道微生物群落更为丰富,代谢特征也更为独特。

Richer gut microbiota with distinct metabolic profile in HIV infected Elite Controllers.

机构信息

Department of Medicine Huddinge, Unit of Infectious Diseases, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.

IrsiCaixa & AIDS Unit, Hospital Universitari Germans Trias i Pujol, Universitat Autònoma de Barcelona, Badalona, Spain.

出版信息

Sci Rep. 2017 Jul 24;7(1):6269. doi: 10.1038/s41598-017-06675-1.

Abstract

Gut microbiota dysbiosis features progressive HIV infection and is a potential target for intervention. Herein, we explored the microbiome of 16 elite controllers (EC), 32 antiretroviral therapy naive progressors and 16 HIV negative controls. We found that the number of observed genera and richness indices in fecal microbiota were significantly higher in EC versus naive. Genera Succinivibrio, Sutterella, Rhizobium, Delftia, Anaerofilum and Oscillospira were more abundant in EC, whereas Blautia and Anaerostipes were depleted. Additionally, carbohydrate metabolism and secondary bile acid synthesis pathway related genes were less represented in EC. Conversely, fatty acid metabolism, PPAR-signalling and lipid biosynthesis proteins pathways were enriched in EC vs naive. The kynurenine pathway of tryptophan metabolism was altered during progressive HIV infection, and inversely associated with microbiota richness. In conclusion, EC have richer gut microbiota than untreated HIV patients, with unique bacterial signatures and a distinct metabolic profile which may contribute to control of HIV.

摘要

肠道微生物失调是 HIV 感染的特征,也是潜在的干预靶点。在此,我们对 16 名精英控制者(EC)、32 名未接受抗逆转录病毒治疗的进展者和 16 名 HIV 阴性对照者的微生物组进行了研究。我们发现,EC 组粪便微生物群中观察到的属数量和丰富度指数明显高于未治疗组。EC 组中,产琥珀酸菌属、萨特氏菌属、根瘤菌属、德氏菌属、厌氧杆菌属和颤螺菌属的丰度更高,而布劳特氏菌属和拟杆菌属的丰度则较低。此外,EC 组碳水化合物代谢和次级胆汁酸合成途径相关基因的表达减少。相反,脂肪酸代谢、过氧化物酶体增殖物激活受体信号和脂质生物合成蛋白途径在 EC 中比在未治疗组中更丰富。色氨酸代谢的犬尿氨酸途径在 HIV 感染进展过程中发生改变,且与微生物群的丰富度呈负相关。总之,EC 拥有比未经治疗的 HIV 患者更丰富的肠道微生物群,具有独特的细菌特征和不同的代谢特征,这可能有助于控制 HIV。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7af3/5524949/f7d3808456b7/41598_2017_6675_Fig1_HTML.jpg

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