ArticleNature communications2024
Profiling the colonic mucosal response to fecal microbiota transplantation identifies a role for GBP5 in colitis in humans and mice.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 16 citations in OpenAlex.
- Microbial engraftment and immune regulation during fecal microbiota transplantation and immune checkpoint inhibitor therapy.Nature communications · 2026Review
- Gut microbiota in health and disease.Molecular biomedicine · 2026Review
- Crohn's Disease: From Immune Dysregulation to Intestinal Damage.Inflammation · 2026Review
- Fecal microbiota transplantation reduces inflammation and modulates gene expression in HIV-infected double humanized-BLT (dHu-BLT) mice on antiretroviral therapy.Frontiers in immunology · 2026Article
- Fecal microbiota transplantation in ulcerative colitis: mucosal immune mechanisms and precision microbiota therapy.Frontiers in immunology · 2026Review
- Recent Advancement of Fecal Microbiota Transplantation in the Treatment of Ulcerative Colitis- A Review.Current medicinal chemistry · 2026Review
- Microbiota transplant therapy in inflammatory bowel disease: advances and mechanistic insights.Gut microbes · 2025Review
- Guanylate-binding protein 5: a promising biomarker and therapeutic target.Infection and immunity · 2025Review
- JAK2 Inhibitors and Emerging Therapies in Graft-Versus-Host Disease: Current Perspectives and Future Directions.Biomedicines · 2025Review
- Role of guanylate-binding protein 5 in inflammatory diseases, immune diseases, cancers, and its potential therapeutic implications.Inflammopharmacology · 2025Review
- STAT1 mediates the pro-inflammatory role of GBP5 in colitis.Communications biology · 2025Article
- CGRPβ suppresses the pathogenesis of ulcerative colitis via the immunoproteasome.Scientific reports · 2025Article
- Fecal Microbiota Transplantation for Attention-Deficit/Hyperactivity Disorder: Mechanisms, Evidence, and Future Directions.International journal of general medicine · 2025Review
- Fundamental and emerging insights into innate and adaptive immunity in inflammatory bowel diseases.Frontiers in immunology · 2025Review
- Diminished Immune Response and Elevated Abundance in Gut Microbe Dubosiella in Mouse Models of Chronic Colitis with GBP5 Deficiency.Biomolecules · 2024Article
- Machine learning-based identification of an immunotherapy-related signature to enhance outcomes and immunotherapy responses in melanoma.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
Abstract
Host molecular responses to fecal microbiota transplantation (FMT) in ulcerative colitis are not well understood. Here, we profile the human colonic mucosal transcriptome prior to and following FMT or placebo to identify molecules regulated during disease remission. FMT alters the transcriptome above the effect of placebo (n = 75 vs 3 genes, q < 0.05), including modulation of structural, metabolic and inflammatory pathways. This response is attributed to responders with no consistency observed in non-responders. Regulated pathways in responders include tight junctions, calcium signalling and xenobiotic metabolism. Genes significantly regulated longitudinally in responders post-FMT could discriminate them from responders and non-responders at baseline and non-responders post-FMT, with GBP5 and IRF4 downregulation being associated with remission. Female mice with a deletion of GBP5 are more resistant to developing colitis than their wild-type littermates, showing higher colonic IRF4 phosphorylation. The colonic mucosal response discriminates UC remission following FMT, with GBP5 playing a detrimental role in colitis.
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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.