HIV感染中的肠道菌群组成变化:起因、影响、及潜在干预手段


Title:
Altered gut microbiome composition in HIV infection: causes, effects and potential intervention

DOI:
10.1097/COH.0000000000000429

Abstract:
Aim of this review is to summarize the alterations occurring in gut microbiome composition after HIV infection, and to underline how intestinal dysbiosis can affect immune homeostasis, immune recovery, and persisting immune activation under antiretroviral therapy (ART). Many interventions have been suggested, mostly with inconclusive results. Recent evidence showed that gut microbiota from HIV-infected patients harbor reproducible differences compared to uninfected individuals. In this line, there is growing evidence that alterations in gut ecology during HIV infection correlate with persistence of immune defects and chronic inflammation. A reduced microbial diversity in feces of HIV-infected patients is highly associated with microbial translocation and monocyte activation markers; moreover, changes in mucosa-associated bacteria correlate with inflammation and T-cell activation. Studying the human host-microbiota interaction suggests that the consequences of HIV infection on microbial composition can influence immune status in HIV patients. ART induces microbiome changes that are independent of HIV infection, and some imply that ART may enhance dysbiosis. Studies and trials evaluated the effects of administering probiotics and prebiotics, finding a potential benefit on inflammation markers and immune cell activation. Emerging data on fecal microbial transplantation need to be assessed with further studies.

All Authors:
Alessandra Bandera,Ilaria De Benedetto,Giorgio Bozzi,Andrea Gori

First Authors:
Alessandra Bandera

Correspondence:
Andrea Gori

内容要点:

HIV感染患者的肠道菌群组成与未感染者显著不同,HIV感染期间的肠道生态改变与免疫缺陷及慢性炎症的持续存在相关。 HIV感染患者的粪便菌群多样性降低与菌群易位及单核细胞活化标记物高度相关。粘膜相关细菌的改变与炎症及T细胞活化显著相关。抗逆转录病毒治疗(ART)可独立于HIV感染影响菌群组成,ART可能增强肠道菌群的失调。一些研究及临床试验表明益生菌、益生元具有对炎症标记物及免疫细胞活化的潜在益处。

Copyright ©2014-2023 罗宁生物 版权所有

All rights reserved Rhonin Biosciences Co.,Ltd.

蜀ICP备15016352号-1