ArticleNature microbiology2024
Altered microbial bile acid metabolism exacerbates T cell-driven inflammation during graft-versus-host disease.
Article in Nature microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Gut microbiota metabolites in the immunoregulation of enteritis: research progress.Frontiers in immunology · 2025Pooled it
- The gut microbiome in graft-versus-host disease: mechanisms of immune modulation and therapeutic approaches.Gut microbes · 2026Review
- Subclinical cholestasis is a hallmark of gut dysbiosis causing resistance to cancer immunotherapy.Cancer cell · 2026Article
- The Role of the Gut Microbiota in Allogeneic Hematopoietic Cell Transplantation.American journal of hematology · 2026Review
- Specific bile acids can elicit the type-I interferon response through the cGAS-STING pathway.Cell communication and signaling : CCS · 2026Article
- Crosstalk between CD8+ T cells and systemic bile acid metabolism shapes antiviral immunity and immunopathology.JCI insight · 2026Article
- The gut microbiome in solid-organ and haematopoietic-stem-cell transplantation.Nature reviews. Microbiology · 2026Review
- Peptide hormones and bile acids shaping immune tolerance of the liver: implications and applications.Protein & cell · 2026Review
- The intestinal microbiota as a key modulator of acute graft-versus-host disease.Nature reviews. Cancer · 2026Review
- Differential effects of two common GVHD prophylaxis regimens on the gut microbiome: Results from the BMT CTN 1801 study.bioRxiv : the preprint server for biology · 2026Article
- Pre-Administration of Akkermansia Muciniphila Prevents the Development of Severe Acute Graft-Versus-Host Disease in Systemic Organs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PURE-seq integrates FACS and PIP-seq for single-cell genomics of ultra-rare cells.Nature communications · 2026Article
- Microbial metabolic memory in inflammatory bowel disease: microbiota-derived metabolites, host-microbe reprogramming, and relapse susceptibility.Frontiers in microbiology · 2026Review
- Microbial transformation of secondary bile acids: roles in gut ecology and autoimmune diseases.Frontiers in immunology · 2026Review
- Gut microbial bile salt hydrolase as a metabolic gatekeeper in digestive homeostasis and disease.Frontiers in immunology · 2026Review
- Host-microbial co-metabolites: from biogenesis to immunomodulation and implications for health and disease.Frontiers in immunology · 2026Review
- Knowledge, attitude and practice regarding metabolic complication management after solid organ transplantation among medical staff in China.Frontiers in public health · 2026Article
- Gastrointestinal acute graft versus host disease: a translational perspective from pathogenesis to precision prevention and treatment.Frontiers in immunology · 2026Review
- Acute gastrointestinal graft-versus-host disease is associated with reductions of secondary bile acids following allogeneic hematopoietic cell transplantation.Frontiers in microbiology · 2026Article
- Effect of fecal microbiota transplantation on gut microbiota functional profile in recipients of allogeneic hematopoietic cell transplantation.Gut microbes · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
31 authors at 6 institutions in 2 countries.
Funding
Abstract
Microbial transformation of bile acids affects intestinal immune homoeostasis but its impact on inflammatory pathologies remains largely unknown. Using a mouse model of graft-versus-host disease (GVHD), we found that T cell-driven inflammation decreased the abundance of microbiome-encoded bile salt hydrolase (BSH) genes and reduced the levels of unconjugated and microbe-derived bile acids. Several microbe-derived bile acids attenuated farnesoid X receptor (FXR) activation, suggesting that loss of these metabolites during inflammation may increase FXR activity and exacerbate the course of disease. Indeed, mortality increased with pharmacological activation of FXR and decreased with its genetic ablation in donor T cells during mouse GVHD. Furthermore, patients with GVHD after allogeneic hematopoietic cell transplantation showed similar loss of BSH and the associated reduction in unconjugated and microbe-derived bile acids. In addition, the FXR antagonist ursodeoxycholic acid reduced the proliferation of human T cells and was associated with a lower risk of GVHD-related mortality in patients. We propose that dysbiosis and loss of microbe-derived bile acids during inflammation may be an important mechanism to amplify T cell-mediated diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.