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Microbiome alterations and host-pathogen interactions in paratuberculosis: A one health perspective
Ankush Dhillon1, Prabhati Yadav1, Saurabh Gupta1
1Department of Biotechnology, GLA University, Mathura, Uttar Pradesh, India.
Veterinary Microbiology
|February 24, 2026
Summary
Mycobacterium avium subsp. paratuberculosis (MAP) causes Johne's disease (JD) by disrupting the gut microbiome, leading to dysbiosis. Understanding these MAP-microbiome interactions offers insights into chronic inflammation and pathogen persistence in both animals and humans.
Area of Science:
- Veterinary Medicine
- Microbiology
- Immunology
- One Health
Background:
- Paratuberculosis, caused by Mycobacterium avium subsp. paratuberculosis (MAP), is a chronic infection with significant economic and public health impacts.
- MAP evades host immunity and alters the gut microbiome, causing dysbiosis that worsens disease progression.
- Johne's disease (JD) serves as a paradigm for chronic infections, involving microbial imbalance, immune escape, and pathogen survival.
Purpose of the Study:
- To review evidence on MAP-induced microbiome alterations and their impact on host-pathogen interactions, immune responses, and metabolism in ruminants.
- To explore the link between MAP infection, gut dysbiosis, and chronic inflammatory diseases across veterinary and human health (One Health approach).
- To identify diagnostic and therapeutic opportunities for microbiome-based interventions in JD.
Main Methods:
- Literature review evaluating molecular, immunological, and microbiome data on MAP infection in ruminants.
- Analysis of MAP-induced changes in microbial diversity, specific bacterial taxa, and metabolic pathways.
- Synthesis of findings within the One Health framework, connecting ruminant JD to human inflammatory bowel diseases.
Main Results:
- JD-associated dysbiosis is characterized by reduced microbial diversity, depleted butyrate producers, and enriched pro-inflammatory bacteria.
- Microbiome alterations may serve as early diagnostic signs and targets for interventions like probiotics or prebiotics.
- MAP-microbiome interactions mirror immune evasion and persistence strategies seen in other intracellular pathogens.
Conclusions:
- MAP-induced dysbiosis is central to JD pathogenesis, immune evasion, and pathogen persistence.
- Understanding these interactions offers translational opportunities for diagnosing and treating chronic inflammatory conditions in both animals and humans.
- Standardized methodologies and multi-omics approaches are needed to clarify the temporal relationship between dysbiosis and MAP infection.
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