# Microbiome–mycotoxin interactions and probiotic strategies: implications for gut health and cancer

**Authors:** Alice N. Mafe, Dietrich Büsselberg

PMC · DOI: 10.3389/fnut.2026.1783295 · 2026-02-25

## TL;DR

This review explores how mycotoxins harm gut health and cancer risk, and how probiotics and gut microbes can help reduce these effects.

## Contribution

The paper provides a novel synthesis of recent findings on microbiome–mycotoxin interactions and probiotic strategies to mitigate health risks.

## Key findings

- Gut microbes can biotransform mycotoxins using enzymes like de-epoxidases and lactonases.
- Probiotics can restore gut barrier function and reduce inflammation caused by mycotoxins.
- Mycotoxin-induced dysbiosis affects short-chain fatty acid production and cancer-related pathways like NF-κB and IL-6.

## Abstract

This structured, hypothesis-driven narrative review examines how mycotoxins, pervasive food contaminants, disrupt intestinal microbial balance, epithelial barrier integrity, xenobiotic metabolism, and carcinogenic signaling. Emerging evidence indicates that bidirectional interactions between the gut microbiome and mycotoxins modulate these effects, with microbial detoxification enzymes influencing toxin metabolism, immune responses, and epithelial resilience. However, the mechanistic understanding of microbiome–mycotoxin interplay remains incomplete, particularly regarding enzymatic pathways, microbial metabolites, and cancer-associated signaling. This review synthesizes recent (2016–2025) mechanistic studies on gut microbiota–mediated mycotoxin biotransformation, enzymatic detoxification, and probiotic interventions as strategies to mitigate mycotoxin-induced gut and cancer-related damage, focusing on key dietary toxins such as aflatoxin B₁, deoxynivalenol, zearalenone, ochratoxin A, fumonisins, and patulin. Evidence indicates that microbial enzymes, including de-epoxidases, lactonases, and reductases, contribute to mycotoxin biotransformation, while probiotics can enhance epithelial barrier function, restore microbial ecosystem balance, and modulate immune responses through toxin binding, competitive exclusion, and anti-inflammatory actions. The review further highlights the strain-specific nature of detoxification, the impact of mycotoxin-induced dysbiosis on short-chain fatty acid production and inflammation, and the modulation of cancer-related pathways including NF-κB, STAT3, and IL-6. Finally, it provides an integrated framework linking microbial mechanisms, bioactive microorganisms, and regulatory considerations, identifies critical knowledge gaps, and outlines mechanistically informed probiotic strategies for mitigating mycotoxin exposure and its associated health risks.

Graphical abstract created in BioRender. Busselberg, D. (2025). https://app.biorender.com/illustrations/6927c7314322ab4a209c929f.Infographic illustrating sources of mycotoxin exposure such as moldy seeds and corn, the impact on gut microbes and dysbiosis, associated detoxification enzyme mechanisms, and probiotic actions leading to improved health outcomes like a healthy gut, reduced inflammation, and lower cancer risk.

Graphical abstract created in BioRender. Busselberg, D. (2025). https://app.biorender.com/illustrations/6927c7314322ab4a209c929f.

## Linked entities

- **Chemicals:** deoxynivalenol (PubChem CID 40024), zearalenone (PubChem CID 5281576), ochratoxin A (PubChem CID 442530), patulin (PubChem CID 4696)
- **Diseases:** cancer (MONDO:0004992)

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, STAT3 (signal transducer and activator of transcription 3) [NCBI Gene 6774] {aka ADMIO, ADMIO1, APRF, HIES}
- **Diseases:** carcinogenic (MESH:D011230), inflammation (MESH:D007249), cancer (MESH:D009369)
- **Chemicals:** short-chain fatty acid (MESH:D005232), fumonisins (MESH:D037341), zearalenone (MESH:D015025), ochratoxin A (MESH:C025589), aflatoxin B1 (MESH:D016604), deoxynivalenol (MESH:C007262), patulin (MESH:D010365)

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12975935/full.md

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Source: https://tomesphere.com/paper/PMC12975935