ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020
Glucosylceramide production maintains colon integrity in response to Bacteroides fragilis toxin-induced colon epithelial cell signaling.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- A systemic review of the role of enterotoxic Bacteroides fragilis in colorectal cancer.Neoplasia (New York, N.Y.) · 2022Pooled it
- Microbiomics: Novel Biomarkers of Colorectal Cancer Diagnosis and Prognosis.Diagnostics (Basel, Switzerland) · 2026Review
- Central Roles of Glucosylceramide in Driving Cancer Pathogenesis.International journal of molecular sciences · 2025Review
- The mesenteric adipokine SFRP5 alleviated intestinal epithelial apoptosis improving barrier dysfunction in Crohn's disease.iScience · 2024Article
- How ceramides affect the development of colon cancer: from normal colon to carcinoma.Pflugers Archiv : European journal of physiology · 2024Review
- The diverse roles of sphingolipids in inflammatory bowel disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Review
- Entero-toxigenicCell cycle (Georgetown, Tex.) · 2024Article
- Analysis of oxidized glucosylceramide and its effects on altering gene expressions of inflammation induced by LPS in intestinal tract cell models.Scientific reports · 2023Article
- Glycolipids in Parkinson's disease: beyond neuronal function.FEBS open bio · 2023Review
- Involvement of Abnormal p-α-syn Accumulation and TLR2-Mediated Inflammation of Schwann Cells in Enteric Autonomic Nerve Dysfunction of Parkinson's Disease: an Animal Model Study.Molecular neurobiology · 2023Article
- Midgut microbiota affects the intestinal barrier by producing short-chain fatty acids inFrontiers in microbiology · 2023Article
- The impact ofmicroPublication biology · 2023Article
- Harnessing the power of sphingolipids: Prospects for acute myeloid leukemia.Blood reviews · 2022Review
- Glycolipid Metabolite β-Glucosylceramide Is a Neutrophil Extracellular Trap-Inducing Ligand of Mincle Released during Bacterial Infection and Inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Glucosylceramide Changes Bacterial Metabolism and Increases Gram-Positive Bacteria through Tolerance to Secondary Bile Acids In Vitro.International journal of molecular sciences · 2022Article
- Novel Insight into the Serum Sphingolipid Fingerprint Characterizing Longevity.International journal of molecular sciences · 2022Article
- Organoids in recapitulating tumorigenesis driven by risk factors: Current trends and future perspectives.International journal of biological sciences · 2022Review
- Intestinal Inflammation and Parkinson's Disease.Aging and disease · 2021Review
- Exploiting unique features of the gut-brain interface to combat gastrointestinal cancer.The Journal of clinical investigation · 2021Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Enterotoxigenic Bacteroides fragilis (ETBF) is a commensal bacterium of great importance to human health due to its ability to induce colitis and cause colon tumor formation in mice through the production of B. fragilis toxin (BFT). The formation of tumors is dependent on a pro-inflammatory signaling cascade, which begins with the disruption of epithelial barrier integrity through cleavage of E-cadherin. Here, we show that BFT increases levels of glucosylceramide, a vital intestinal sphingolipid, both in mice and in colon organoids (colonoids) generated from the distal colons of mice. When colonoids are treated with BFT in the presence of an inhibitor of glucosylceramide synthase (GCS), the enzyme responsible for generating glucosylceramide, colonoids become highly permeable, lose structural integrity, and eventually burst, releasing their contents into the extracellular matrix. By increasing glucosylceramide levels in colonoids via an inhibitor of glucocerebrosidase (GBA, the enzyme that degrades glucosylceramide), colonoid permeability was reduced, and bursting was significantly decreased. In the presence of BFT, pharmacological inhibition of GCS caused levels of tight junction protein 1 (TJP1) to decrease. However, when GBA was inhibited, TJP1 levels remained stable, suggesting that BFT-induced production of glucosylceramide helps to stabilize tight junctions. Taken together, our data demonstrate a glucosylceramide-dependent mechanism by which the colon epithelium responds to BFT.
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Registered trials
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