Pathogens Outcompeted by E. coli Nissle 1917 and Beneficial Conditions

Overview

E. coli Nissle 1917 (EcN) is a unique, non-pathogenic Escherichia coli strain first isolated during World War I by German physician Alfred Nissle in 1917. Alfred Nissle, a German researcher, found it in a soldier who remained free of dysentery during a severe outbreak in the Shigella-contaminated Balkans.^[1] Unlike pathogenic E. coli, EcN lacks virulence genes that cause disease, yet it carries extra genetic fitness factors that give it a competitive edge in the gut.^[2] Over the last century, EcN has become one of the most studied probiotic strains, used to prevent or treat digestive disorders and now inspiring new medical applications.

How E. coli Nissle 1917 Outcompetes Pathogens

EcN Strategy	Mechanism
Microcins	EcN produces special microcins (notably MccM and MccH47) and uniquely, EcN’s microcins are “siderophore-microcins,” meaning they piggyback on iron-scavenging molecules (siderophores) to enter rival bacteria by a “Trojan Horse” strategy.[3] Pathogens unwittingly uptake these iron-mimicking complexes, only to be attacked from within. This gives EcN a key advantage in the crowded gut by selectively wiping out closely related pathogens like Salmonella.[4]
Biofilm formation	EcN not only forms its own biofilm but can also disrupt pathogenic biofilms. Studies found EcN’s cell-free supernatant can prevent and break down biofilms of Pseudomonas aeruginosa, a dangerous opportunistic pathogen.[5] Without harming beneficial bacteria or the pathogen’s free-living cells, EcN’s secretions specifically targeted Pseudomonas biofilm structure, even reducing the extracellular DNA that holds biofilms together.
Secreted anti-virulence factors	Remarkably, EcN can interfere with pathogens even without direct contact. Laboratory studies revealed that EcN released something ( >30 kDa in size) that inhibited the invasion of human cells by invasive bacteria like Shigella, Salmonella, Yersinia,Listeria and even Legionella, despite not killing them outright.[6] The invasive ability dropped by approximately 70% when EcN was present, and even a microcin-deficient EcN mutant still blocked invasion effectively– pointing to a secreted anti-virulence factor.[7]
Immune modulation	EcN also rallies the host’s immune defenses. It has broad immunomodulatory effects on both innate and adaptive immunity. For instance, EcN has been shown to stimulate increased production of IgA and IgM antibodies in the gut mucosa.[8] IgA in particular helps neutralize pathogens at the mucosal surface. EcN can induce anti-inflammatory cytokines and reinforce the intestinal lining’s immune tolerance.

How Does E. coli Nissle 1917 Work?

EcN essentially acts on three fronts: it directly suppresses pathogens, it fortifies the gut environment, and it engages the host immune system. The interplay of these actions results in the therapeutic outcomes.

Establishes a Foothold

It adheres to the mucus layer and possibly to intestinal epithelial cells using its fimbriae and other adhesion factors (EcN has fimbrial adhesins that help it stick).^[9] It forms microcolonies in the gut mucosa. This creates a physical barrier that blocks pathogen attachment sites and helps reinforce the mucosal barrier.^[10] EcN colonization is typically temporary (weeks to months), but while present, it occupies niches that could otherwise harbor harmful microbes.

Releases Antimicrobial Compounds

EcN begins secreting its microcins and other bacteriocins into the surroundings.^[11] These diffuse through the gut content and specifically target competing Gram-negative bacteria. For example, microcin M and H47 will attach to iron receptors on susceptible E. coli or Salmonella and kill those cells, reducing pathogen load. At the same time, EcN pumps out siderophores to snag iron, undercutting any pathogen’s attempt to multiply.^[12]

Interferes with Pathogen Behavior

EcN also sheds larger proteins and metabolites that can travel and affect pathogen behavior. For instance, a secreted factor can bind to invading bacteria and somehow prevent their invasion into the gut lining.^[13] Other molecules might degrade signaling compounds (quorum molecules), so pathogens can’t coordinate an attack or form resilient communities.

Dialogues with the Immune System

Components of EcN (like its cell wall, flagella, and DNA CpG motifs) are recognized by the body’s immune sensors (Toll-like receptors, etc.). But unlike a pathogen that causes excessive inflammation, EcN triggers a calibrated immune reaction, boosting protective immunity without pathological inflammation.^[14] EcN induces IgA secretion into the gut lumen, which can neutralize toxins and microbes.^[15] It can also upregulate anti-inflammatory mediators (e.g., IL-10) and strengthen the epithelial barrier (increasing mucin production and anti-microbial peptides from the host). This immune modulation helps resolve chronic inflammation in conditions like ulcerative colitis and improves overall readiness to fight infections.^[16]

Pathogens outcompeted by E. coli Nissle 1917

EcN’s competitive mechanisms are not just theoretical, as there is concrete evidence that it outcompetes or inhibits a broad array of pathogens known to cause gastrointestinal (and even systemic) infections. The following table summarises documented pathogens and parasites that EcN can inhibit or outcompete, based on experimental or clinical evidence.

Pathogen	Disease / Context	Mechanisms of Inhibition by EcN
Enteropathogenic/enterotoxigenic/enterohemorrhagic E. coli (EPEC, ETEC, EHEC)	Various diarrheagenic E. coli strains	EcN inhibits pathogenic E. coli through the formation of biofilms on epithelial surfaces, which occupy adhesion sites, thus preventing pathogens from adhering and establishing infection.[17] EcN produces microcins, such as MccM and MccH47, under iron-limited conditions. These microcins disrupt the pathogens’ cell membranes, and EcN also outcompetes them for iron, reducing their growth.[18]
Adherent-invasive E. coli (AIEC) and commensal E. coli	Crohn’s disease‑associated AIEC and non‑pathogenic strains	EcN restricts the growth of both pathogenic AIEC and commensal E. coli by producing siderophore-conjugated microcins, such as MccM and MccH47, which are internalized by these bacteria via their siderophore receptors.[19]
Salmonella enterica (including S. Typhimurium)	Gastroenteritis and systemic infection	EcN combats Salmonella by producing the microcin MccM, which inhibits the bacteria’s growth under iron-limited conditions.[20] EcN competes for iron via multiple siderophore systems, which limits the availability of iron for Salmonella and prevents its expansion.[21][22] EcN’s biofilm formation on intestinal surfaces further blocks Salmonella from attaching and invading the epithelium.
Yersinia enterocolitica	Enteritis	EcN reduces the invasion of Yersinia into human intestinal cells by secreting inhibitory factors, which act independently of the microcins, and by outcompeting Yersinia for available adhesion sites on epithelial cells.[23] EcN may also prevent biofilm formation, further hindering Yersinia’s ability to colonize the gut.[24]
Shigella flexneri	Dysentery/shigellosis	EcN inhibits the invasion of Shigella flexneri into intestinal epithelial cells through the secretion of factors that interfere with the pathogen’s adhesion and invasion machinery.[25] EcN’s biofilm formation on intestinal surfaces prevents Shigella from attaching, thus reducing its ability to establish infection.
Legionella pneumophila	Legionnaires’ disease	EcN reduces the ability of Legionella pneumophila to invade human epithelial cells in the respiratory tract.[26] While EcN does not affect the viability of Legionella, it blocks its ability to infect lung epithelial cells.
Listeria monocytogenes	Invasive listeriosis	EcN inhibits Listeria monocytogenes from invading epithelial cells through the secretion of inhibitory factors, which block the pathogen’s adhesion and invasion machinery.[27][28] EcN’s biofilm formation on intestinal surfaces prevents Listeria from colonizing epithelial cells and establishing infection.[29]
Pseudomonas aeruginosa	Nosocomial infections	EcN’s cell-free supernatants inhibit Pseudomonas aeruginosa’s biofilm formation and even disperse mature biofilms.[30] This effect is due to the downregulation of quorum-sensing proteins (LasI, RhlR), which are essential for Pseudomonas to initiate virulence and biofilm maturation, thus limiting its ability to establish infections.
Clostridium perfringens	Gas gangrene, food poisoning	EcN inhibits the growth of Clostridium perfringens by competing for essential nutrients, thereby limiting the bacteria’s ability to proliferate.[31] EcN suppresses the production of alpha-toxins and NetB toxins, which are key virulence factors for C. perfringens, by reducing inflammation and nutrient availability.
Campylobacter jejuni	Campylobacteriosis	Pre-treatment of human colonic cells with EcN reduces the invasion of Campylobacter jejuni, and no intracellular C. jejuni is recovered after 24 hours of co-culture with EcN.[32] By preventing pathogen attachment and invasion, EcN significantly limits C. jejuni colonization.
Klebsiella pneumoniae	Opportunistic infections, carbapenem-resistant Enterobacteriaceae	EcN outcompetes Klebsiella pneumoniae for nutrients in cecal filtrate medium after 24 hours. This competitive advantage disappears when EcN is cultured in glucose or fucose-supplemented media, demonstrating the role of nutrient competition in pathogen inhibition.[33]
Candida albicans	Candidiasis and gut mycosis	EcN co-culture decreases Candida albicans abundance over time, preventing damage to epithelial cells. EcN alters Candida’s filamentous growth and microcolony formation, which suggests direct fungicidal activity.[34] Through these mechanisms, EcN reduces the pathogen’s ability to cause infection and damage tissue.
Enterococcus faecalis	Catheter-associated urinary tract infection (CAUTI)	EcN forms probiotic biofilms on mannoside-functionalized silicone catheters, which prevent the colonization of Enterococcus faecalis.[35] By occupying available adhesion sites and outcompeting the pathogen, EcN reduces the risk of catheter-associated infections.[36]
Entamoeba histolytica	Amebic dysentery	EcN reduces the viability of Entamoeba histolytica by inducing trophozoite rounding and vacuolization, likely due to oxidative stress.[37] EcN exposure also leads to the production of reactive oxygen species (ROS), which damage the pathogen and prevent its survival in the gut.

Clinical Benefits of E. coli Nissle 1917

EcN has been widely researched and utilized in clinical settings for its therapeutic potential in managing a variety of gastrointestinal and systemic conditions. EcN’s clinical benefits arise from its ability to outcompete pathogens, modulate the immune system, improve gut health, and restore microbial balance. EcN has shown effectiveness in the management of inflammatory bowel diseases (such as ulcerative colitis), irritable bowel syndrome (IBS), chronic constipation, and acute diarrhea.^[38] It has also demonstrated a role in preventing urinary tract infections (UTIs), improving immune responses, and even serving as a potential adjunct in anti-tumor therapies.^[39] The clinical benefits of EcN are primarily attributed to its biofilm formation, immune modulation, microcin production, and its ability to outcompete harmful pathogens in the gut. As a result, EcN helps in reducing inflammation, alleviating symptoms, and restoring gut barrier integrity.

Table of Clinical Benefits of EcN

Clinical Benefit	Condition / Disease Context	Mechanisms of Action
Maintenance of Remission in Ulcerative Colitis	Ulcerative colitis (UC)	EcN supports UC remission by improving gut barrier integrity, enhancing epithelial tight junctions, and reducing inflammatory markers.[40] It also stimulates antimicrobial peptide production and produces biofilms that outcompete harmful pathogens.[41]
Alleviation of Symptoms in Irritable Bowel Syndrome	Irritable Bowel Syndrome (IBS)	EcN alleviates IBS symptoms by restoring microbial balance in the gut, modulating immune responses (increased IL-10 and decreased IL-1β), and reducing inflammation.[42] It also helps in balancing the gut microbiome.
Treatment of Chronic Constipation	Chronic constipation	EcN improves motility and stool consistency by modulating gut microbiota, increasing short-chain fatty acid (SCFA) production, and promoting smoother muscle function.[43] These effects lead to improved bowel movement frequency.
Shortened Recovery from Acute Diarrhea in Children	Acute gastroenteritis in children (e.g., rotavirus diarrhea)	EcN reduces the severity and duration of acute diarrhea by improving gut barrier function, enhancing immune responses, and restoring a healthy microbiome.[44] It also shortens recovery time and reduces virus shedding in rotavirus-infected animals.
Reduction in Severity of Rotavirus Diarrhea	Rotavirus-induced diarrhea	EcN modulates the immune response by increasing plasmacytoid dendritic cell frequency, enhancing natural killer (NK) cell activity, and inducing a balanced cytokine production profile.[45] It reduces diarrhea severity and virus shedding.
Prevention of Urinary Tract Infections (UTIs)	Catheter-associated urinary tract infection (CAUTI)	EcN forms biofilms on catheters that prevent colonization by Enterococcus faecalis, thereby preventing CAUTIs.[46] It also competes with pathogens for adhesion sites and prevents biofilm formation of harmful bacteria.[47]
Prophylaxis of Acute Respiratory Infections in Neonates	Acute respiratory infections in preterm neonates	EcN reduces the frequency of acute respiratory infections and hospitalizations by modulating the gut microbiota, which influences the immune system (gut-lung axis).[48][x] EcN also enhances systemic immunity and supports gut barrier integrity.
Anti-tumor Applications	Adjunct therapy for cancer treatment (colon cancer)	EcN is being explored for its ability to colonize tumors, survive hypoxic conditions, and outcompete other bacteria in inflammatory sites.[49] Engineered EcN strains are being tested as vehicles for delivering cancer therapeutics directly to tumor sites.[50]

Safety Considerations

EcN has an excellent safety record in infants, children, adults, and the elderly, with most people experiencing no side effects beyond occasional mild, short-lived digestive upset.^[51] It is non-pathogenic and lacks key virulence traits, and although it carries the colibactin (pks) gene cluster, extensive in vitro and animal studies show no genotoxic or mutagenic effects. However, researchers continue to monitor this area. As with any live probiotic, clinicians should exercise caution in severely immunocompromised or critically ill patients (e.g., those with neutropenia, in the ICU, or with major mucosal disruption), because the theoretical risk of bloodstream infection or translocation is higher and requires medical supervision. EcN responds sensitively to many antibiotics and requires proper storage, meaning its benefits rely on viable cells, appropriate timing around antibiotic courses, and successful colonisation.^[52] Despite these considerations, EcN continues to demonstrate a strongly favourable risk–benefit profile in its approved clinical uses.

Research Feed

References

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22. Microcins mediate competition among Enterobacteriaceae in the inflamed gut.. Sassone-Corsi, M., Nuccio, P., Liu, H., Hernandez, D., Vu, C. T., Takahashi, A. A., Edwards, R. A., & Raffatellu, M. (2016).. (Nature, 540(7632), 280.)
23. Antibacterial MccM as the Major Microcin in Escherichia coli Nissle 1917 against Pathogenic Enterobacteria.. Ma, Y., Fu, W., Hong, B., Wang, X., Jiang, S., & Wang, J. (2023).. (International Journal of Molecular Sciences, 24(14), 11688.)
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26. The probiotic Escherichia coli strain Nissle 1917 interferes with invasion of human intestinal epithelial cells by different enteroinvasive bacterial pathogens.. Altenhoefer A, Oswald S, Sonnenborn U, Enders C, Schulze J, Hacker J, Oelschlaeger TA.. (FEMS Immunol Med Microbiol. 2004 Apr 9;40(3):223-9.)
27. The probiotic Escherichia coli strain Nissle 1917 interferes with invasion of human intestinal epithelial cells by different enteroinvasive bacterial pathogens.. Altenhoefer A, Oswald S, Sonnenborn U, Enders C, Schulze J, Hacker J, Oelschlaeger TA.. (FEMS Immunol Med Microbiol. 2004 Apr 9;40(3):223-9.)
28. The non-pathogenic Escherichia coli strain Nissle 1917 – features of a versatile probiotic.. Sonnenborn, U., & Schulze, J. (2009).. (Microbial Ecology in Health and Disease, 21(3–4), 122–158.)
29. The non-pathogenic Escherichia coli strain Nissle 1917 – features of a versatile probiotic.. Sonnenborn, U., & Schulze, J. (2009).. (Microbial Ecology in Health and Disease, 21(3–4), 122–158.)
30. Escherichia coli Nissle 1917 inhibits biofilm formation and mitigates virulence in Pseudomonas aeruginosa.. Aljohani, A. M., Alhubail, M., Ledder, R. G., A., C., & McBain, A. J. (2023).. (Frontiers in Microbiology, 14, 1108273.)
31. Yanlong Jiang, Qingke Kong, Kenneth L. Roland, Amanda Wolf, Roy Curtiss. Multiple effects of Escherichia coli Nissle 1917 on growth, biofilm formation, and inflammation cytokines profile of Clostridium perfringens type A strain CP4. (Pathogens and Disease, Volume 70, Issue 3, April 2014, Pages 390–400)
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33. Klebsiella pneumoniae l-Fucose Metabolism Promotes Gastrointestinal Colonization and Modulates Its Virulence Determinants.. Hudson, A. W., Barnes, A. J., Bray, A. S., Ornelles, D. A., & Zafar, M. A. (2022).. (Infection and Immunity, 90(10), e00206-22.)
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37. Amebicidal Activity of Escherichia coli Nissle 1917 Against Entamoeba histolytica.. Moura-Oliveira, V., S Oliveira, F. M., M Moreno, O. L., Ferreira, J. R., Szawka, R. E., Campideli-Santana, A. C., Teles, J., A Capettini, L. S., Martins, F. S., & Gomes, M. A. (2025).. (Microorganisms, 13(4), 828.)
38. Role and mechanisms of action of Escherichia coli Nissle 1917 in the maintenance of remission in ulcerative colitis patients: An update.. Scaldaferri, F., Gerardi, V., Mangiola, F., Lopetuso, L. R., Pizzoferrato, M., Petito, V., Papa, A., Stojanovic, J., Poscia, A., Cammarota, G., & Gasbarrini, A. (2016).. (World Journal of Gastroenterology, 22(24), 5505.)
39. Towards Understanding Tumour Colonisation by Probiotic Bacterium E. Coli Nissle 1917.. Radford, G. A., Vrbanac, L., Worthley, D. L., Wright, J. A., Hasty, J., & Woods, S. L. (2024).. (Cancers, 16(17), 2971.)
40. Role and mechanisms of action of Escherichia coli Nissle 1917 in the maintenance of remission in ulcerative colitis patients: An update.. Scaldaferri, F., Gerardi, V., Mangiola, F., Lopetuso, L. R., Pizzoferrato, M., Petito, V., Papa, A., Stojanovic, J., Poscia, A., Cammarota, G., & Gasbarrini, A. (2016).. (World Journal of Gastroenterology, 22(24), 5505.)
41. Role and mechanisms of action of Escherichia coli Nissle 1917 in the maintenance of remission in ulcerative colitis patients: An update.. Scaldaferri, F., Gerardi, V., Mangiola, F., Lopetuso, L. R., Pizzoferrato, M., Petito, V., Papa, A., Stojanovic, J., Poscia, A., Cammarota, G., & Gasbarrini, A. (2016).. (World Journal of Gastroenterology, 22(24), 5505.)
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44. The probiotic Escherichia coli strain Nissle 1917 (EcN) stops acute diarrhoea in infants and toddlers.. Henker, J., Laass, M., Blokhin, B. M., Bolbot, Y. K., Maydannik, V. G., Elze, M., Wolff, C., & Schulze, J. (2007).. (European Journal of Pediatrics, 166(4), 311.)
45. Escherichia coli Nissle 1917 protects gnotobiotic pigs against human rotavirus by modulating plasmacytoid dendritic and natural killer cell responses.. Vlasova, A. N., Shao, L., Kandasamy, S., Fischer, D. D., Rauf, A., Langel, S. N., Chattha, K. S., Kumar, A., Huang, C., Rajashekara, G., & Saif, L. J. (2016).. (European Journal of Immunology, 46(10), 2426.)
46. A Comprehensive Review of Progress in Preventing Urinary Infections Associated with the Use of Urinary Catheters: A Dual Analysis of Publications and Patents.. Corrado, B., Cammarano, A., Iacono, S. D., Renzi, E., Moretta, R., Mercurio, M. E., Ascione, L., Cummaro, A., Meglio, C., & Nicolais, L. (2025).. (Infectious Disease Reports, 17(3), 64.)
47. A Comprehensive Review of Progress in Preventing Urinary Infections Associated with the Use of Urinary Catheters: A Dual Analysis of Publications and Patents.. Corrado, B., Cammarano, A., Iacono, S. D., Renzi, E., Moretta, R., Mercurio, M. E., Ascione, L., Cummaro, A., Meglio, C., & Nicolais, L. (2025).. (Infectious Disease Reports, 17(3), 64.)
48. Prophylaxis of acute respiratory infections via improving the immune system in late preterm newborns with E. coli strain Nissle 1917: a controlled pilot trial.. Aryayev, M.L., Senkivska, L.I., Bredeleva, N.K. et al.. (Pilot Feasibility Stud 4, 79 (2018).)
49. Towards Understanding Tumour Colonisation by Probiotic Bacterium E. Coli Nissle 1917.. Radford, G. A., Vrbanac, L., Worthley, D. L., Wright, J. A., Hasty, J., & Woods, S. L. (2024).. (Cancers, 16(17), 2971.)
50. The non-pathogenic Escherichia coli strain Nissle 1917 – features of a versatile probiotic.. Sonnenborn, U., & Schulze, J. (2009).. (Microbial Ecology in Health and Disease, 21(3–4), 122–158.)
51. The probiotic Escherichia coli strain Nissle 1917 (EcN) stops acute diarrhoea in infants and toddlers.. Henker, J., Laass, M., Blokhin, B. M., Bolbot, Y. K., Maydannik, V. G., Elze, M., Wolff, C., & Schulze, J. (2007).. (European Journal of Pediatrics, 166(4), 311.)
52. Towards Understanding Tumour Colonisation by Probiotic Bacterium E. Coli Nissle 1917.. Radford, G. A., Vrbanac, L., Worthley, D. L., Wright, J. A., Hasty, J., & Woods, S. L. (2024).. (Cancers, 16(17), 2971.)