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
Review
. 2024 Mar 20:15:1288856.
doi: 10.3389/fmicb.2024.1288856. eCollection 2024.

Bacteroides and NAFLD: pathophysiology and therapy

Jun Zhang #  1   2 , Jing Zhou #  1 , Zheyun He  3   4 , Hongshan Li  1   4
Affiliations
Review

Bacteroides and NAFLD: pathophysiology and therapy

Jun Zhang et al. Front Microbiol. .

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic liver condition observed globally, with the potential to progress to non-alcoholic steatohepatitis (NASH), cirrhosis, and even hepatocellular carcinoma. Currently, the US Food and Drug Administration (FDA) has not approved any drugs for the treatment of NAFLD. NAFLD is characterized by histopathological abnormalities in the liver, such as lipid accumulation, steatosis, hepatic balloon degeneration, and inflammation. Dysbiosis of the gut microbiota and its metabolites significantly contribute to the initiation and advancement of NAFLD. Bacteroides, a potential probiotic, has shown strong potential in preventing the onset and progression of NAFLD. However, the precise mechanism by which Bacteroides treats NAFLD remains uncertain. In this review, we explore the current understanding of the role of Bacteroides and its metabolites in the treatment of NAFLD, focusing on their ability to reduce liver inflammation, mitigate hepatic steatosis, and enhance intestinal barrier function. Additionally, we summarize how Bacteroides alleviates pathological changes by restoring the metabolism, improving insulin resistance, regulating cytokines, and promoting tight-junctions. A deeper comprehension of the mechanisms through which Bacteroides is involved in the pathogenesis of NAFLD should aid the development of innovative drugs targeting NAFLD.

Keywords: Bacteroides; NAFLD; intestinal barrier; liver inflammation; steatosis.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Potential mechanisms underlying the attenuation of hepatic steatosis by Bacteroides in NAFLD. Bacteroides and its active ingredient, bacterial extracellular vesicles (BEVs), alleviate hepatic steatosis and associated insulin resistance. AMPK, adenosine monophosphate-activated protein kinase; mTOR, mechanistic target of rapamycin; SREBP-1, sterol regulatory element-binding protein-1; ChREBP, carbohydrate response element-binding protein; ACC, acetyl-CoA carboxylase; FAS, fatty acid synthase; BEVs, bacterial extracellular vesicles; BSH, bile salt hydrolase; TGR5, takeda G protein-coupled receptor 5; FXR, farnesoid X receptor; DPP-4, dipeptidyl peptidase-4; GLP-1, glucagon-like peptide-1; IR, insulin resistance; PPARα, peroxisome proliferator-activated receptor α.
FIGURE 2
FIGURE 2
Potential mechanisms contributing to the prevention of hepatic inflammation by Bacteroides in NAFLD. Bacteroides regulated inflammation and immune response in the livers of NAFLD patients. The current focus on the mechanisms underlying the improvement of hepatic inflammation by Bacteroides primarily revolves around the production of inflammatory factors and LPS and TLR4 signaling. IL-22, interleukin-22; IFN-γ, interferon-γ; IL-10, interleukin-10; LPS, lipopolysaccharide; TNF-α, tumor necrosis factor-α; PSA, polysaccharide A; TLR4, toll-like receptor 4; NF-κB, nuclear factor-κB; IL-1β, interleukin-1β.
FIGURE 3
FIGURE 3
Potential mechanisms involved in enhancing the intestinal barrier function by Bacteroides in NAFLD. Bacteroides and its metabolites enhance the barrier function of the intestine through modulating intestinal inflammatory factors, improving the expression of tight-junction proteins, and restoring intestinal dysbiosis. DC, dendritic cells; F. prausnitzii, Faecalibacterium prausnitzii; IL-10, interleukin-10; ZO-1, zonula occludens-1; PSA, polysaccharide A; IL-17, interleukin 17; TJ, tight-junction.
See this image and copyright information in PMC

Similar articles

See all similar articles

References

    1. Abdelnabi M. N., Flores Molina M., Soucy G., Quoc-Huy Trinh V., Bedard N., Mazouz S., et al. (2022). Sex-dependent hepatoprotective role of IL-22 receptor signaling in non-alcoholic fatty liver disease-related fibrosis. Cell Mol. Gastroenterol. Hepatol. 14 1269–1294. 10.1016/j.jcmgh.2022.08.001 - DOI - PMC - PubMed
    1. Amiri P., Arefhosseini S., Bakhshimoghaddam F., Jamshidi Gurvan H., Hosseini S. A. (2022). Mechanistic insights into the pleiotropic effects of butyrate as a potential therapeutic agent on NAFLD management: a systematic review. Front. Nutr. 9:1037696. 10.3389/fnut.2022.1037696 - DOI - PMC - PubMed
    1. An L., Wirth U., Koch D., Schirren M., Drefs M., Koliogiannis D., et al. (2022). The role of gut-derived lipopolysaccharides and the intestinal barrier in fatty liver diseases. J. Gastrointest Surg. 26 671–683. 10.1007/s11605-021-05188-7 - DOI - PMC - PubMed
    1. Aoki R., Onuki M., Hattori K., Ito M., Yamada T., Kamikado K., et al. (2021). Commensal microbe-derived acetate suppresses NAFLD/NASH development via hepatic FFAR2 signalling in mice. Microbiome 9:188. 10.1186/s40168-021-01125-7 - DOI - PMC - PubMed
    1. Arab J. P., Karpen S. J., Dawson P. A., Arrese M., Trauner M. (2017). Bile acids and nonalcoholic fatty liver disease: molecular insights and therapeutic perspectives. Hepatology 65 350–362. 10.1002/hep.28709 - DOI - PMC - PubMed

Grants and funding

The authors declare that financial support was received for the research, authorship, and/or publication of this article. This work was supported by the Zhejiang Provincial Natural Science Foundation of China under Grant No. LY23H290004, the Ningbo Natural Science Foundation, Project ID: 2022J242, the Major Special Science and Technology Project of Ningbo City (#2022Z128), National Administration of Traditional Chinese Medicine - Zhejiang Provincial Administration of Traditional Chinese Medicine Joint Construction Technology Plan (GZY-ZJ-KJ-23092), Zhejiang Province Traditional Chinese Medicine Science and Technology Plan (2022ZB332), and the Project of NINGBO Leading Medical and Health Discipline, Project Number: 2022Z01.

LinkOut - more resources

-