Antibacterial MccM as the Major Microcin in Escherichia coli Nissle 1917 against Pathogenic Enterobacteria Original paper
Researched by:
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Divine Aleru
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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.
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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 More
Researched by:
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Divine Aleru
ID
Divine Aleru
Read More
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.
Divine Aleru
What was studied?
This study investigated how the probiotic Escherichia coli Nissle 1917 microcin MccM contributes to antibacterial activity against pathogenic enterobacteria, with a primary focus on Salmonella species. The researchers examined whether MccM acts as the dominant antimicrobial factor by comparing wild-type EcN with mutants lacking microcin genes and with a strain engineered to overexpress MccM. This work aimed to clarify how EcN exerts microbiome-mediated antagonism within the gut and to define the specific molecular contributions of MccM to competitive fitness, colonization resistance, and inflammatory modulation.
Who was studied?
The study used laboratory strains of Escherichia coli Nissle 1917, including wild type, three CRISPR-generated microcin knockout mutants, and an engineered MccM overproducer. These were tested against clinically relevant pathogens, including EHEC O157:H7, Salmonella enterica, and Salmonella Typhimurium. In vitro cell line models involving murine RAW264.7 macrophages and epithelial cells were used to evaluate inflammatory responses, adhesion, and invasion. The design enabled a controlled evaluation of how microcin-dependent interactions shape microbial competition and host immune signaling.
Most important findings
The study showed that Escherichia coli Nissle 1917 microcin MccM is the major determinant of EcN’s antagonistic effect against Salmonella. MccM knockout sharply reduced EcN’s ability to inhibit Salmonella growth, while overexpression of mcmA produced stronger inhibition than wild-type EcN. EcN::mcmA reduced Salmonella adhesion and invasion far more effectively, lowering invasion by over fifty percent and enhancing impairment of adhesion relative to wild type. The engineered strain also suppressed LPS-induced IL1β, TNFα, and IL6 expression in macrophages, indicating an added immunomodulatory effect. Increased siderophore production in EcN::mcmA supported a competitive iron sequestration mechanism, aligning MccM activity with a Trojan horse strategy through siderophore-linked uptake pathways. These findings highlight a clear microbiome signature in which MccM shapes pathogen exclusion and host response within an iron limited intestinal environment.
Key implications
The results show that enhancing Escherichia coli Nissle 1917 microcin MccM expression can significantly improve probiotic suppression of Salmonella, offering a strong foundation for engineered microbiome-targeted therapies. The data suggest that MccM-driven iron competition and translocation mechanisms represent actionable targets for preventing colonization by enteric pathogens. The observed reduction in inflammatory cytokine production also indicates that MccM-enhanced EcN may help limit pathogen-induced inflammation. These insights expand the functional profile of EcN and support precision engineering of probiotic strains to reinforce colonization resistance and improve clinical outcomes.