{"title":"Gut Microbiota in Intestinal and Liver Disease.","authors":"Rheinallt M Jones, Andrew S Neish","doi":"10.1146/annurev-pathol-030320-095722","DOIUrl":null,"url":null,"abstract":"<p><p>It is known that the gut microbiota, the numerically vast and taxonomically diverse microbial communities that thrive in a symbiotic fashion within our alimentary tract, can affect the normal physiology of the gastrointestinal tract and liver. Further, disturbances of the microbiota community structure from both endogenous and exogenous influences as well as the failure of host responsive mechanisms have been implicated in a variety of disease processes. Mechanistically, alterations in intestinal permeability and dysbiosis of the microbiota can result in inflammation, immune activation, and exposure to xenobiotic influences. Additionally, the gut and liver are continually exposed to small molecule products of the microbiota with proinflammatory, gene regulatory, and oxidative properties. Long-term coevolution has led to tolerance and incorporation of these influences into normal physiology and homeostasis; conversely, changes in this equilibrium from either the host or the microbial side can result in a wide variety of immune, inflammatory, metabolic, and neoplastic intestinal and hepatic disorders.</p>","PeriodicalId":50753,"journal":{"name":"Annual Review of Pathology-Mechanisms of Disease","volume":"16 ","pages":"251-275"},"PeriodicalIF":28.4000,"publicationDate":"2021-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1146/annurev-pathol-030320-095722","citationCount":"52","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annual Review of Pathology-Mechanisms of Disease","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1146/annurev-pathol-030320-095722","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2020/11/24 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"PATHOLOGY","Score":null,"Total":0}
引用次数: 52
Abstract
It is known that the gut microbiota, the numerically vast and taxonomically diverse microbial communities that thrive in a symbiotic fashion within our alimentary tract, can affect the normal physiology of the gastrointestinal tract and liver. Further, disturbances of the microbiota community structure from both endogenous and exogenous influences as well as the failure of host responsive mechanisms have been implicated in a variety of disease processes. Mechanistically, alterations in intestinal permeability and dysbiosis of the microbiota can result in inflammation, immune activation, and exposure to xenobiotic influences. Additionally, the gut and liver are continually exposed to small molecule products of the microbiota with proinflammatory, gene regulatory, and oxidative properties. Long-term coevolution has led to tolerance and incorporation of these influences into normal physiology and homeostasis; conversely, changes in this equilibrium from either the host or the microbial side can result in a wide variety of immune, inflammatory, metabolic, and neoplastic intestinal and hepatic disorders.
期刊介绍:
The Annual Review of Pathology: Mechanisms of Disease is a scholarly journal that has been published since 2006. Its primary focus is to provide a comprehensive overview of recent advancements in our knowledge of the causes and development of significant human diseases. The journal places particular emphasis on exploring the current and evolving concepts of disease pathogenesis, as well as the molecular genetic and morphological changes associated with various diseases. Additionally, the journal addresses the clinical significance of these findings.
In order to increase accessibility and promote the broad dissemination of research, the current volume of the journal has transitioned from a gated subscription model to an open access format. This change has been made possible through the Annual Reviews' Subscribe to Open program, which allows all articles published in this volume to be freely accessible to readers. As part of this transition, all articles in the journal are published under a Creative Commons Attribution (CC BY) license, which encourages open sharing and use of the research.