ArticleMucosal immunology2016
The goblet cell-derived mediator RELM-β drives spontaneous colitis in Muc2-deficient mice by promoting commensal microbial dysbiosis.
Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 2 of them syntheses that pooled it.
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Who cites it
73 citing papers in PubMed, 2 syntheses or guidelines pooled it, 109 citations in OpenAlex.
- Influence of Alcohol on the Intestinal Immune System.Alcohol research : current reviews · 2025Pooled it
- Pooled it
- Immune Stimulation Using a Gut Microbe-Based Immunotherapy Reduces Disease Pathology and Improves Barrier Function in Ulcerative Colitis.Frontiers in immunology · 2018Trial
- Microbiome-driven alterations in tryptophan metabolism contribute to behavioral comorbidities in the Muc2 knockout mouse model of chronic colitis.Gut microbes · 2026Article
- Roles for specialized secretory epithelial cells in inflammatory bowel disease.Current opinion in gastroenterology · 2026Review
- A Nutrient-Dense Diet with Optimal Protein Level Restores Goblet Cells and Alleviates Microbial Dysbiosis in a Mouse Model of Colitis.The Journal of nutrition · 2026Article
- Butyrate extends health and lifespan in mice with mitochondrial deficiency.Nature communications · 2026Article
- Lanatoside C ameliorates DSS-induced colitis with improved intestinal barrier integrity and reduced M1 macrophage polarization.Scientific reports · 2026Article
- Context-dependent roles of resistin-like molecule β in mucosal defense and inflammatory diseases.Frontiers in immunology · 2026Review
- From mucus secretion to immune surveillance: the evolving roles of goblet cells in intestinal homeostasis and inflammation.Frontiers in immunology · 2026Review
- Context-dependent roles of the gut microbiome in food allergy tolerance versus sensitization.Gut microbes · 2025Review
- Cathelicidin regulates goblet cell mucus secretion and mucus-associated proteins inGut microbes · 2025Article
- [Toxicity of lunar dust simulant exposure via the digestive system: Microbiota dysbiosis and multi-organ injury].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Article
- Therapeutic targeting of the NOTCH1 and neddylation pathways in T cell acute lymphoblastic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Wnt/β-catenin maintains epithelial IL-33 in the colonic stem and progenitor cell niche and drives its induction in colitis.Mucosal immunology · 2025Article
- The Impact in Intestines and Microbiota in BALB/c Mice Through Consumption of Milk Fermented by Potentially Probiotic Lacticaseibacillus casei SJRP38 and Limosilactobacillus fermentum SJRP43.Probiotics and antimicrobial proteins · 2025Article
- Functional evaluation of synbiotic combination ofCurrent research in food science · 2025Article
- Oral administration of curcumin and quercetin nanoparticles can improve ulcerative colitis by regulating intestinal microorganisms.Frontiers in nutrition · 2025Article
- Pancreastatin Inhibition Alters the Colonic Epithelial Cells Profile in a Sex-Dependent Manner.International journal of molecular sciences · 2024Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Intestinal goblet cells are potentially key players in controlling susceptibility to ulcerative colitis (UC). Although impaired mucin (Muc2) production by goblet cells increases microbial stimulation of the colonic mucosa, goblet cells secrete other mediators that may influence or promote UC development. Correspondingly, Muc2-deficient ((-/-)) mice develop spontaneous colitis, concurrent with the dramatic upregulation of the goblet cell mediator, resistin-like molecule-beta (RELM-β). Testing RELM-β's role, we generated Muc2(-/-)/Retnlb(-/-) mice, finding that RELM-β deficiency significantly attenuated colitis development and symptoms compared with Muc2(-/-) mice. RELM-β expression in Muc2(-/-) mice strongly induced the production/secretion of the antimicrobial lectin RegIIIβ, that exerted its microbicidal effect predominantly on Gram-positive Lactobacillus species. Compared with Muc2(-/-)/Retnlb(-/-) mice, this worsened intestinal microbial dysbiosis with a selective loss of colonic Lactobacilli spp. in Muc2(-/-) mice. Orally replenishing Muc2(-/-) mice with murine Lactobacillus spp., but not with a probiotic formulation containing several human Lactobacillus spp. (VSL#3), ameliorated their spontaneous colitis in concert with increased production of short-chain fatty acids. These studies demonstrate that the goblet cell mediator RELM-β drives colitis in Muc2(-/-) mice by depleting protective commensal microbes. The ability of selective commensal microbial replacement to ameliorate colitis suggests that personalized bacterial therapy may prove beneficial for treatment of UC.
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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.