ArticleFrontiers in microbiology2022
Microbial metabolites indole derivatives sensitize mice to D-GalN/LPS induced-acute liver failure
Article in Frontiers in microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Lacticaseibacillus paracasei 36 attenuates D-GalN/LPS-induced acute liver injury in mice via suppressing the TLR4/NF-κB/MAPK pathway and NLRP3 inflammasome activation through modulating the intestinal microbiota.Journal of advanced research · 2026Article
- Animal models accurately representing acute liver failure (Review).International journal of molecular medicine · 2026Review
- Integrative network pharmacology and machine learning identify potential targets of indole-3-lactic acid in colorectal cancer.PloS one · 2026Article
- Gut microbial metabolites of amino acids in liver diseases.Gut microbes · 2025Review
- Multifaceted Role of Microbiota-Derived Indole-3-Acetic Acid in Human Diseases and Its Potential Clinical Application.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Indole-3-Lactic Acid Inhibits Doxorubicin-Induced Ferroptosis Through Activating Aryl Hydrocarbon Receptor/Nrf2 Signalling Pathway.Journal of cellular and molecular medicine · 2025Article
- Calycosin inhibits hepatocyte apoptosis in acute liver failure by suppressing the TLR4/NF-κB pathway: An in vitro study.Immunity, inflammation and disease · 2023Article
- Crosstalk between lactic acid and immune regulation and its value in the diagnosis and treatment of liver failure.Open life sciences · 2023Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Acute liver failure (ALF) is a clinical condition with many causes, fast progression, and a poor prognosis. Previous research has indicated that microbial factors have a role in ALF, but a clear picture has yet to emerge. Methods: To investigate the specific involvement of microbial metabolites in ALF development, we pretreated D-GalN/LPS-induced ALF mice with indole derivatives, an influential class of gut microbial metabolites. Results: Contrary to their typical role as anti-inflammatory agents in the host, indole-3-acetic acid (IAA), indole-3-lactic acid (ILA), and indolepropionic acid (IPA) gavage sensitize mice to D-GalN/LPS-induced-ALF with a rapid rise in serum transaminases and histologic lesion. For a clearer picture, we performed comprehensive analysis for the IAA therapy. IAA markedly amplified inflammatory response and cellular damage. The transcriptome analysis indicated the participation of the TNF-α/NF-κB signaling pathway. The structure of gut microbiota in ileum and the expression of Toll-like receptor 2 (Tlr2) in the liver were also significantly changed. Discussion: In conclusion, IAA pretreatment can exacerbate D-GalN/LPS-induced ALF via probable Tlr2/NF-κB pathway involvement and ileac dysbiosis characterized by enriched gram-positive genus with potential pathogenesis. Microbial metabolites IAA may aggravate individual susceptibility to D-GalN/LPS-induced ALF. Further investigation of the underlying mechanism is needed, and intervention with indole derivatives and related commensal species should be undertaken with caution.
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