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The Immunologic Role of Gut Microbiota in Patients with Chronic HBV Infection

Hepatitis B can cause acute or chronic liver damage due to hepatitis B virus (HBV) infection. Cirrhosis or hepatocellular carcinoma (HCC) caused by chronic HBV infection often leads to increased mortality. However, the gut and liver have the same embryonic origin; therefore, a close relationship mus...

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Detalles Bibliográficos
Autores principales: Yang, Ruilin, Xu, Yao, Dai, Zhifeng, Lin, Xuhong, Wang, Huichao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6083645/
https://www.ncbi.nlm.nih.gov/pubmed/30148173
http://dx.doi.org/10.1155/2018/2361963
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author Yang, Ruilin
Xu, Yao
Dai, Zhifeng
Lin, Xuhong
Wang, Huichao
author_facet Yang, Ruilin
Xu, Yao
Dai, Zhifeng
Lin, Xuhong
Wang, Huichao
author_sort Yang, Ruilin
collection PubMed
description Hepatitis B can cause acute or chronic liver damage due to hepatitis B virus (HBV) infection. Cirrhosis or hepatocellular carcinoma (HCC) caused by chronic HBV infection often leads to increased mortality. However, the gut and liver have the same embryonic origin; therefore, a close relationship must exist in terms of anatomy and function, and the gut microbiota plays an important role in host metabolic and immune modulation. It is believed that structural changes in the gut microbiota, bacterial translocation, and the resulting immune injury may affect the occurrence and development of liver inflammation caused by chronic HBV infection based on the in-depth cognition of the concept of the “gut-liver axis” and the progress in intestinal microecology. This review aims to summarize and discuss the immunologic role of the gut microbiota in chronic HBV infection.
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spelling pubmed-60836452018-08-26 The Immunologic Role of Gut Microbiota in Patients with Chronic HBV Infection Yang, Ruilin Xu, Yao Dai, Zhifeng Lin, Xuhong Wang, Huichao J Immunol Res Review Article Hepatitis B can cause acute or chronic liver damage due to hepatitis B virus (HBV) infection. Cirrhosis or hepatocellular carcinoma (HCC) caused by chronic HBV infection often leads to increased mortality. However, the gut and liver have the same embryonic origin; therefore, a close relationship must exist in terms of anatomy and function, and the gut microbiota plays an important role in host metabolic and immune modulation. It is believed that structural changes in the gut microbiota, bacterial translocation, and the resulting immune injury may affect the occurrence and development of liver inflammation caused by chronic HBV infection based on the in-depth cognition of the concept of the “gut-liver axis” and the progress in intestinal microecology. This review aims to summarize and discuss the immunologic role of the gut microbiota in chronic HBV infection. Hindawi 2018-07-25 /pmc/articles/PMC6083645/ /pubmed/30148173 http://dx.doi.org/10.1155/2018/2361963 Text en Copyright © 2018 Ruilin Yang et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Yang, Ruilin
Xu, Yao
Dai, Zhifeng
Lin, Xuhong
Wang, Huichao
The Immunologic Role of Gut Microbiota in Patients with Chronic HBV Infection
title The Immunologic Role of Gut Microbiota in Patients with Chronic HBV Infection
title_full The Immunologic Role of Gut Microbiota in Patients with Chronic HBV Infection
title_fullStr The Immunologic Role of Gut Microbiota in Patients with Chronic HBV Infection
title_full_unstemmed The Immunologic Role of Gut Microbiota in Patients with Chronic HBV Infection
title_short The Immunologic Role of Gut Microbiota in Patients with Chronic HBV Infection
title_sort immunologic role of gut microbiota in patients with chronic hbv infection
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6083645/
https://www.ncbi.nlm.nih.gov/pubmed/30148173
http://dx.doi.org/10.1155/2018/2361963
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