Related Experiment Video

Updated: May 31, 2026

Assessment of Intestinal Transcytosis of Neonatal Escherichia coli Bacteremia Isolates
08:32

Assessment of Intestinal Transcytosis of Neonatal Escherichia coli Bacteremia Isolates

Published on: February 17, 2023

Enterococcus faecalis metalloprotease compromises epithelial barrier and contributes to intestinal inflammation

Natalie Steck1, Micha Hoffmann, Irina G Sava

  • 1Chair for Biofunctionality, ZIEL-Research Center for Nutrition and Food Science, CDD Center for Diet and Disease, Technische Universität München, Freising-Weihenstephan, Germany.

Gastroenterology
|June 25, 2011
PubMed
Abstract

Insights

Enterococcus faecalis gelatinase (GelE) contributes to chronic intestinal inflammation by degrading E-cadherin and impairing epithelial barrier integrity in susceptible mice.

Area of Science:

  • Microbiology
  • Immunology
  • Gastroenterology

Background:

  • Matrix metalloproteases (MMPs) play a role in chronic intestinal inflammation.
  • Enterococcus faecalis gelatinase (GelE) is a metalloprotease with a potential role in colitis pathogenesis.

Purpose of the Study:

  • To characterize the role of GelE from E. faecalis in the development of colitis in a mouse model.
  • To investigate the impact of GelE on epithelial barrier function.

Main Methods:

  • Germ-free IL-10-deficient mice were monoassociated with E. faecalis strains (wild-type and GelE-mutant).
  • Epithelial barrier function was assessed by measuring E-cadherin expression, transepithelial electrical resistance (TER), and marker translocation.
  • GelE specificity was confirmed using the MMP inhibitor marimastat.

Main Results:

  • Absence of GelE significantly reduced colonic inflammation in monoassociated IL-10(-/-) mice.
  • GelE was shown to cleave E-cadherin, leading to its degradation.
  • GelE impaired epithelial barrier integrity, evidenced by reduced TER and increased permeability in susceptible mice.

Conclusions:

  • The metalloprotease GelE from E. faecalis contributes to chronic intestinal inflammation.
  • GelE impairs epithelial barrier integrity, exacerbating colitis in susceptible mouse models (IL-10(-/-) and TNF(ΔARE/Wt)).

More Related Videos

Injections of Lipopolysaccharide into Mice to Mimic Entrance of Microbial-derived Products After Intestinal Barrier Breach08:24

Injections of Lipopolysaccharide into Mice to Mimic Entrance of Microbial-derived Products After Intestinal Barrier Breach

Published on: May 2, 2018

Related Concept Videos

Dysbiosis of the Gut Microbiota01:18

Dysbiosis of the Gut Microbiota

The human gut microbiome includes a diverse array of microbial species, including beneficial commensals and opportunistic pathogens, which interact to support host health. These microbes contribute to essential functions such as nutrient metabolism, immune system modulation, and maintenance of intestinal barrier integrity. However, disruptions to this equilibrium—referred to as dysbiosis—can have widespread physiological consequences.Dysbiosis is often characterized by reduced microbial...
Bacterial Gastroenteritis01:18

Bacterial Gastroenteritis

Bacterial gastroenteritis, characterized by diarrhea, abdominal cramps, and vomiting, is often caused by ingestion of contaminated food or water and is frequently associated with pathogenic Escherichia coli strains. These microbes exploit two principal mechanisms to inflict disease.Shiga toxin–producing E. coli, also referred to as STEC—notably O157:H7—release Shiga toxins that target ribosomes, blocking protein synthesis. The B subunit of the toxin binds the host glycolipid receptor...
Clinical Significance of Antibiotic Resistance01:25

Clinical Significance of Antibiotic Resistance

Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within the One...
Amebiasis01:28

Amebiasis

Entamoeba histolytica, a protozoan parasite, is responsible for intestinal and extraintestinal amebiasis. Though a significant proportion of infections remain asymptomatic, approximately 50 million individuals annually are estimated to present with clinical disease, resulting in up to 100,000 deaths globally. The disease burden is disproportionately high in regions with lower socioeconomic status, such as parts of India, Africa, Mexico, and Latin America.Etiology and TransmissionThe infective...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...