Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2015 Apr;5(4):83-85.
doi: 10.1002/cld.453. Epub 2015 May 7.

Microbiome-Immune Interactions and Liver Disease

James H Tabibian  1 , Cyril Varghese  2 , Steven P O'Hara  1 , Nicholas F LaRusso  1
Affiliations

Microbiome-Immune Interactions and Liver Disease

James H Tabibian et al. Clin Liver Dis (Hoboken). 2015 Apr.
No abstract available

PubMed Disclaimer

Conflict of interest statement

Potential conflict of interest: Nothing to report.

Figures

Figure 1
Figure 1
Conceptual schema of the gut microbiome‐liver interaction in hepatobiliary disease. A growing body of basic, translational, and clinical evidence suggests that the intestinal microbiome and microbially derived molecules (1) interact with each other and with the host and may be involved in the pathogenesis of chronic hepatobiliary disease. Various potential mechanisms may be involved, depending on the particular disease condition as well as other known (e.g. host genotype, diet, age, exposure to antibiotics, and stage of disease) and unknown factors. For example, in a number of hepatobiliary diseases and in most patients with advanced cirrhosis, there is (2) dysfunction of the epithelial barrier (e.g., tight junction disruption through the action of ethanol and other metabolites and pathophysiologic changes), resulting in increased permeability to and enterohepatic circulation of potentially injurious microbial molecules (e.g., lipopolysaccharide). These molecules can (3) bind to cell surface and intracellular pathogen recognition molecules on hepatocytes as well as biliary, endothelial, stellate, Kupffer, and other cells and initiate signal transduction cascades. These cascades culminate in (4) upregulated biosynthesis of cytokines (e.g., interleukins, interferons, and chemokines), which, although aimed at effectuating clearance of the inciting insult, may also lead to hepatobiliary injury (e.g., inflammation, fibrosis, and senescence) and initiation of immune dysregulation (e.g., development of autoimmunity). This may result in (5) induction, modulation, or progression of chronic liver disease. The physiology and dysregulation of this gut‐liver axis and its complex and dynamic interactions are the focus of intense investigation and hold promise for advancing the management of chronic liver disease. [Color figure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]
See this image and copyright information in PMC

References

    1. Consortium HMP. Structure, function and diversity of the healthy human microbiome. Nature 2012;486:207‐214. - PMC - PubMed
    1. Round JL, Mazmanian SK. The gut microbiota shapes intestinal immune responses during health and disease. Nat Rev Immunol 2009;9:313‐323. - PMC - PubMed
    1. Hösel M, Broxtermann M, Janicki H, Esser K, Arzberger S, Hartmann P, et al. Toll‐like receptor 2‐mediated innate immune response in human nonparenchymal liver cells toward adeno‐associated viral vectors. Hepatology 2012;55:287‐297. - PubMed
    1. Wang B, Trippler M, Pei R, Lu M, Broering R, Gerken G, et al. Toll‐like receptor activated human and murine hepatic stellate cells are potent regulators of hepatitis C virus replication. J Hepatol 2009;51:1037‐1045. - PubMed
    1. Yokoyama T, Komori A, Nakamura M, Takii Y, Kamihira T, Shimoda S, et al. Human intrahepatic biliary epithelial cells function in innate immunity by producing IL‐6 and IL‐8 via the TLR4‐NF‐kappaB and ‐MAPK signaling pathways. Liver Int 2006;26:467‐476. - PubMed