Escherichia coli Nissle 1917 inhibits biofilm formation and mitigates virulence in Pseudomonas aeruginosa Original paper
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Microbes
Microbes
Microbes, short for microorganisms, are tiny living organisms that are ubiquitous in the environment, including on and inside the human body. They play a crucial role in human health and disease, functioning within complex ecosystems in various parts of the body, such as the skin, mouth, gut, and respiratory tract. The human microbiome, which is […]
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Divine Aleru
Read MoreI am a biochemist with a deep curiosity for the human microbiome and how it shapes human health, and I enjoy making microbiome science more accessible through research and writing. With 2 years experience in microbiome research, I have curated microbiome studies, analyzed microbial signatures, and now focus on interventions as a Microbiome Signatures and Interventions Research Coordinator.
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
I am a biochemist with a deep curiosity for the human microbiome and how it shapes human health, and I enjoy making microbiome science more accessible through research and writing. With 2 years experience in microbiome research, I have curated microbiome studies, analyzed microbial signatures, and now focus on interventions as a Microbiome Signatures and Interventions Research Coordinator.
What was studied?
This study investigated the biofilm inhibition and virulence mitigation effects of Escherichia coli Nissle 1917 (EcN) against Pseudomonas aeruginosa. The researchers tested cell-free supernatants (CFS) from EcN and other bacterial strains for their ability to inhibit biofilm formation and disrupt existing biofilms of P. aeruginosa. The study also explored the protective effect of EcN CFS in a Galleria mellonella larvae model, alongside proteomic analysis to determine the molecular interactions involved in the biofilm suppression.
Who was studied?
The study focused on Pseudomonas aeruginosa, a pathogenic bacterium known for its ability to form biofilms that contribute to chronic infections. The study used several P. aeruginosa strains, including PAO1, SNP0614, and LYT-4, to assess the antibiofilm activity of EcN. The Galleria mellonella larval model was also used to evaluate the in vivo virulence mitigation properties of EcN CFS.
Most important findings
EcN CFS significantly inhibited the formation of P. aeruginosa biofilms without affecting the planktonic growth of the bacteria. It also disrupted mature biofilms, reducing extracellular DNA (eDNA) accumulation, a key component of biofilm structure. The biofilm inhibition was dose-dependent, with a minimum biofilm inhibitory concentration (MBIC) of 25%. Proteomic analysis revealed that EcN CFS downregulated several P. aeruginosa proteins involved in motility, quorum sensing, and biofilm formation. The active antibiofilm factors were heat-labile and proteinaceous, with molecular weights between 30 and 100 kDa.
Key implications
The results suggest that E. coli Nissle 1917 could be a potential therapeutic agent for mitigating P. aeruginosa infections by targeting biofilm formation and virulence factors. The protective effect observed in the Galleria mellonella model highlights its potential for further clinical development as a probiotic or therapeutic agent. The study also provides insights into the molecular mechanisms behind the anti-biofilm activity of EcN, which could aid in developing strategies for combating biofilm-associated infections in clinical settings.
Escherichia coli Nissle 1917 (EcN) is a rare, non-pathogenic strain of E. coli discovered during World War I from a soldier who did not get dysentery while others did. Unlike harmful E. coli, EcN acts as a probiotic: it settles in the gut, competes with bad bacteria for food and space, produces natural antimicrobials, and even helps strengthen the gut barrier.