Target intelligence / Profile preview

Escherichia coli strain Nissle 1917 (EcN)

Target
EcN
Molecular classification
Probiotic, Gram-negative bacterium, Microbiome-based therapeutic
01

Overview

Escherichia coli strain Nissle 1917 (EcN) is a non-pathogenic, Gram-negative probiotic bacterium that has been used for over a century to treat various gastrointestinal disorders. Originally isolated by Alfred Nissle in 1917, this strain is unique because it lacks common virulence factors and instead possesses fitness factors that allow it to outcompete pathogenic bacteria in the human gut (Wassenaar, 2016). EcN functions by strengthening the intestinal epithelial barrier through the upregulation of tight junction proteins and by inducing the production of antimicrobial peptides like human beta-defensin 2 (Altenhoefer et al., 2004). It also modulates the host immune system by shifting the cytokine balance toward an anti-inflammatory profile, which is particularly beneficial in conditions like ulcerative colitis (Schultz, 2008). In clinical practice, EcN is most notably used for the maintenance of remission in ulcerative colitis, where its efficacy is comparable to the standard-of-care drug mesalazine (Kruis et al., 2004). Beyond its role as a direct therapeutic, EcN is increasingly being utilized in synthetic biology as a chassis for engineered probiotics designed to deliver specific drugs or sense metabolic changes within the microbiota (Landry et al., 2018). While generally considered safe and well-tolerated, its use is contraindicated in severely immunocompromised patients due to the risk of systemic translocation and sepsis (Sonnenborn, 2016). As a living therapeutic, its activity is highly dependent on the host's existing microbiota and can be significantly impaired by the administration of broad-spectrum antibiotics.

Other names
MutaflorE. coli NissleEcNDSM 6601Escherichia coli strain Nissle
02

Mechanism of action

EcN exerts therapeutic effects through competitive exclusion of pathogens, production of microcins (M and H47), induction of human beta-defensin 2 (hBD-2), and stabilization of the intestinal epithelial barrier via upregulation of tight junction proteins like ZO-1 and occludin (Altenhoefer et al., 2004; Ukena et al., 2007).

03

Biological functions

ImmunomodulationIntestinal barrier stabilizationCompetitive exclusionAntimicrobial productionPathogen inhibition
04

Disease associations

Ulcerative colitisInflammatory bowel diseaseIrritable bowel syndromeInfectionDiarrhea
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Safety considerations

Bacteremia in immunocompromised patientsAntibiotic sensitivityHorizontal gene transferGastrointestinal flatulence
06

Interacting drugs

Mesalazine

4 more in the full profile.

07

Biomarkers

Fecal calprotectinHuman beta-defensin 2 (hBD-2)EcN-specific DNA (PCR)Stool cytokine levels

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