ArticleInfection and immunity2015
Enterococcus faecalis Gelatinase Mediates Intestinal Permeability via Protease-Activated Receptor 2.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Features of Gut Microbiome Associated With Responses to Fecal Microbiota Transplantation for Inflammatory Bowel Disease: A Systematic Review.Frontiers in medicine · 2022Pooled it
- Microbial shifts and signatures of long-term remission in ulcerative colitis after faecal microbiota transplantation.The ISME journal · 2017Trial
- Protease-serpin-microbiome interactions in inflammatory bowel disease: toward integrated biomarkers of gut health.Gut microbes · 2026Review
- Iron, Biofilm, and Colorectal Cancer: Mechanistic Insights Into Enterococcus faecalis Pathogenesis.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2026Review
- Metabolic shifts driven by host-microbial interactions.The FEBS journal · 2026Review
- Loss of Fsr quorum sensing promotes biofilm formation and worsens outcomes in enterococcal infective endocarditis.Nature communications · 2026Article
- Virulome over taxonomy: refining the driver-passenger model in colorectal carcinogenesis.Frontiers in cellular and infection microbiology · 2026Review
- Proteases in intestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2026Review
- Microbiome dysbiosis and its modulation in cancer development, prevention and therapy.Frontiers in oncology · 2026Review
- Gastrointestinal microbiota and inflammasomes interplay in health and disease: a gut feeling.Gut · 2025Review
- Cultured bacteria isolated from primary sclerosing cholangitis patient bile induce inflammation and cell death.mSphere · 2025Article
- A Bacteroides fragilis protease activates host PARCell host & microbe · 2025Article
- Enteroendocrine cells: the gatekeepers of microbiome-gut-brain communication.NPJ biofilms and microbiomes · 2025Review
- Identification of a secreted protease frombioRxiv : the preprint server for biology · 2025Article
- Microbiota-targeted strategies in IBD: therapeutic promise of 2'-fucosyllactose and beyond.Therapeutic advances in gastroenterology · 2025Review
- Role of E-cadherin in epithelial barrier dysfunction: implications for bacterial infection, inflammation, and disease pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- The immunomodulatory and antitumor properties of the bacterial metalloprotease Oligopeptidase A are mediated by TLR4/MyD88/TRIF and MAPK signaling pathways.Frontiers in immunology · 2025Article
- Genotypic and phenotypic characterization ofbioRxiv : the preprint server for biology · 2024Article
- Enterococcal-host interactions in the gastrointestinal tract and beyond.FEMS microbes · 2024Review
- Fecal gelatinase does not predict mortality in patients with alcohol-associated hepatitis.Microbial cell (Graz, Austria) · 2024Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
Microbial protease-mediated disruption of the intestinal epithelium is a potential mechanism whereby a dysbiotic enteric microbiota can lead to disease. This mechanism was investigated using the colitogenic, protease-secreting enteric microbe Enterococcus faecalis. Caco-2 and T-84 epithelial cell monolayers and the mouse colonic epithelium were exposed to concentrated conditioned media (CCM) from E. faecalis V583 and E. faecalis lacking the gelatinase gene (gelE). The flux of fluorescein isothiocyanate (FITC)-labeled dextran across monolayers or the mouse epithelium following exposure to CCM from parental or mutant E. faecalis strains indicated paracellular permeability. A protease-activated receptor 2 (PAR2) antagonist and PAR2-deficient (PAR2(-/-)) mice were used to investigate the role of this receptor in E. faecalis-induced permeability. Gelatinase (GelE) purified from E. faecalis V583 was used to confirm the ability of this protease to induce epithelial cell permeability and activate PAR2. The protease-mediated permeability of colonic epithelia from wild-type (WT) and PAR2(-/-) mice by fecal supernatants from ulcerative colitis patients was assessed. Secreted E. faecalis proteins induced permeability in epithelial cell monolayers, which was reduced in the absence of gelE or by blocking PAR2 activity. Secreted E. faecalis proteins induced permeability in the colonic epithelia of WT mice that was absent in tissues from PAR2(-/-) mice. Purified GelE confirmed the ability of this protease to induce epithelial cell permeability via PAR2 activation. Fecal supernatants from ulcerative colitis patients induced permeability in the colonic epithelia of WT mice that was reduced in tissues from PAR2(-/-) mice. Our investigations demonstrate that GelE from E. faecalis can regulate enteric epithelial permeability via PAR2.
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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.