Evidence map›Paper›PMID 42256221›Full record

ReviewFrontiers in cellular and infection microbiology2026

From dysbiosis to precision medicine: targeting the microbial-metabolic axis in IBD management.

John K Giju, Subin John, Amrutha Sivadas, Meera Prabhakar, Krishnakripa K, Damu Sunilkumar, Bipin G Nair, Sanjay Pal, Vidhya Prakash

Abstract readReview
In one paragraph

Review in Frontiers in cellular and infection microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

John K GijuSchool of Biotechnology, Amrita Vishwa Vidyapeetham, Kollam, Kerala, India.
Subin JohnSchool of Biotechnology, Amrita Vishwa Vidyapeetham, Kollam, Kerala, India.
Amrutha SivadasSchool of Biotechnology, Amrita Vishwa Vidyapeetham, Kollam, Kerala, India.
Meera PrabhakarSchool of Biotechnology, Amrita Vishwa Vidyapeetham, Kollam, Kerala, India.
Krishnakripa KSchool of Biotechnology, Amrita Vishwa Vidyapeetham, Kollam, Kerala, India.
Damu SunilkumarThe Ohio State University Wexner Medical Center and Comprehensive Cancer Center, Columbus, OH, United States.
Bipin G NairSchool of Biotechnology, Amrita Vishwa Vidyapeetham, Kollam, Kerala, India.
Sanjay PalSchool of Biotechnology, Amrita Vishwa Vidyapeetham, Kollam, Kerala, India.
Vidhya PrakashSchool of Biotechnology, Amrita Vishwa Vidyapeetham, Kollam, Kerala, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel disease (IBD) is a chronic relapsing inflammatory condition that has a rapidly changing global epidemiology. IBD has been traditionally viewed as a primary immune system dysfunction, but emerging evidence more accurately describes IBD as a perturbance of the intricate balance between host immunity, the intestinal microbiome, and intestinal metabolism. Although genetic and environmental components have long been recognized as contributors, accumulating evidence increasingly highlights the pivotal role of microbial dysbiosis in the pathogenesis of IBD. In patients with IBD, intestinal dysbiosis, which is often characterized by reduced Firmicutes and increased pro-inflammatory bacteria, triggers a cascade of pathogenic events. These pathogenic events include impaired epithelial barrier function, dysregulated immune activation against luminal antigens, and immune reprogramming. Central to these processes are functional changes in microbial metabolism, particularly in pathways involving short-chain fatty acids (SCFAs), bile acids, and redox homeostasis, which critically contribute to the development of chronic mucosal inflammation. The current therapeutic backbone of IBD-including aminosalicylates, biologics, and immunomodulators-largely targets the inflammatory response. However, the challenges such as primary non-response, secondary loss of response, and systemic side effects are often problematic. Consequently, there is an urgent need to develop novel therapeutic and preventive strategies that target the underlying microbial and metabolic causes of the disease rather than modulating immune responses. This review integrates the pathomechanistic implications of the microbiome-metabolic axis in the maintenance of gut homeostasis and its disruption in IBD, with particular emphasis on the global epidemiology of the disease. We further evaluate emerging therapeutic and preventive strategies aimed at restoring the microbiome-metabolic axis, including fecal microbiota transplantation (FMT), probiotic therapy, bacteriophage therapy, and helminth-based therapies. In addition, we explore the potential of advanced approaches such as microbiome engineering and precision genome editing to enable highly personalized therapeutic paradigms. By bridging microbial ecology with clinical pathology, this review highlights the transformative potential of targeting the host-microbiota interface to achieve improved long-term outcomes in IBD.

Indexed as

DysbiosisGastrointestinal MicrobiomeInflammatory Bowel DiseasesProbioticsAnimalsAntimicrobial PeptidesDiet TherapyFatty Acids, VolatileHumansImmunomodulationIntestinal Barrier FunctionPlant PreparationsPrecision MedicineAntimicrobial PeptidesFatty Acids, VolatilePlant PreparationsCrohn’s diseasegut dysbiosisintestinal homeostasismachine learningmetagenomicsprobioticsSCFA (short-chain fatty acid)ulcerative colitis

Identifiers

PMID42256221
PMCPMC13236684

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.