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Updated: Aug 5, 2026

Colonization with Murine pks+ Escherichia coli under Non-Inflammatory Conditions
Published on: March 10, 2026
The diet-microbiota-inflammation axis and colorectal cancer
Konstantinos Kossenas1, Christos Damaskos2, Nikolaos Garmpis3
1Laiko General Hospital, Athens, Greece.
Background:
Colorectal cancer (CRC) is still one of the leading causes of cancer morbidity and mortality worldwide. There is increasing evidence that diet, gut microbiota, microbial metabolites and chronic inflammation are important factors in colorectal carcinogenesis and may provide novel opportunities for prevention, diagnosis and treatment.
Aim:
To provide a comprehensive review of the current evidence on the role of diet, nutrition, microbial metabolism and chronic inflammation in CRC, with emphasis on emerging translational applications including microbiome-based biomarkers and microbiota-targeted therapeutic strategies.
Methods:
A literature search was performed with PubMed, Scopus and the Cochrane Library. Relevant studies on diet-microbiota interactions, microbial metabolites, inflammatory mechanisms, colorectal carcinogenesis, microbiome-derived biomarkers, and microbiota-targeted interventions were identified and reviewed. Preclinical and clinical studies and high quality reviews and meta-analyses were considered.
Results:
Dietary patterns have been shown to have a major impact on the composition and function of the gut microbiota. Rich-fiber diets and short-chain fatty acids (SCFAs) production seem protective against CRC, while western dietary patterns, ultra-processed foods and dysbiosis-associated metabolites promote a pro-inflammatory environment associated with carcinogenesis. Some microorganisms such as Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis and pks-positive Escherichia coli have been associated with CRC by inflammatory, genotoxic and immune-modulatory mechanisms. Recent advances in sequencing technologies and multi-omics approaches have enabled the identification of microbial signatures with potential diagnostic and prognostic value. Moreover, microbiota-targeted interventions such as probiotics, prebiotics, postbiotics, faecal microbiota transplantation, and next-generation microbial therapies have yielded promising preclinical and early clinical results.
Conclusions:
The diet-microbiota-inflammation axis is a key player in colorectal carcinogenesis and a promising target for translational research. Microbiome-based biomarkers and microbiota-targeted therapies may have a role in future precision prevention and personalised management strategies of colorectal cancer despite significant challenges in terms of causation, standardisation and translation into clinical practice.
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