Gut mycobiome dysbiosis in inflammatory bowel disease: a systematic review and meta-analysis
- 1Fundación para la Investigación Biomédica, Instituto de Investigación Sanitaria, Hospital Clínico San Carlos
- 2Departamento de Farmacología, Facultad de Medicina, Universidad de Valencia
- 3Centro de Investigación Biomédica en Red (CIBER) de Enfermedades Hepáticas y Digestivas, Instituto de Salud Carlos III
Abstract
Background: The intestinal mycobiome is increasingly recognized as an important component of host–microbiota interactions in inflammatory bowel disease (IBD), yet its contribution to intestinal immune dysregulation remains incompletely characterized. We aimed to characterize alterations in the intestinal mycobiome in patients with inflammatory bowel disease, including Crohn’s disease and ulcerative colitis, compared with individuals without IBD, focusing on fungal diversity, taxonomic composition, and relative abundance, as well as their potential associations with disease phenotype and inflammatory activity.
Methods: A systematic review and meta-analysis was conducted according to PRISMA 2020 guidelines. PubMed/MEDLINE, Embase, and Cochrane Central Register of Controlled Trials were systematically searched from inception to March 2026, with no language or publication-date restrictions. The review was not prospectively registered. Human studies assessing gut fungal communities by internal transcribed spacer (ITS)-based sequencing or shotgun metagenomics were eligible. Alpha and beta diversity, taxonomic composition, and clinically relevant fungal alterations were extracted. Study quality was assessed independently by two reviewers using the Newcastle–Ottawa Scale (NOS), and quantitative analyses were performed using standardized effect estimates and pooled prevalence.
Results: Twenty-eight studies were included in the qualitative and quantitative synthesis. CD was consistently associated with reduced fungal alpha diversity compared with healthy controls, with a pooled weighted mean difference in Shannon diversity of −0.84 (p<0.001), whereas the reduction in UC was more modest (−0.31, p=0.04). Fungal beta diversity consistently differed between IBD and healthy controls. Expansion of Candida spp. was the most reproducible taxonomic alteration, occurring in 82.1% of analyzed cohorts, while depletion of Saccharomyces cerevisiae was reported in 71.4%. Malassezia enrichment was also associated with mucosal inflammation and CARD9-related immune responses. Cross-kingdom interactions involving Candida , Escherichia coli , and Serratia marcescens further highlighted potential fungal–bacterial mechanisms underlying persistent inflammation. Persistent fungal dysbiosis despite clinical remission supported the concept of a “mycobiotic scar.”
Conclusion: IBD is characterized by substantial disruption of the intestinal mycobiome, particularly in CD, with reduced fungal diversity, expansion of potentially pathogenic Candida spp., and depletion of protective fungal taxa. These alterations may contribute to immune dysregulation and therapeutic refractoriness and support the mycobiome as a potential source of biomarkers and therapeutic targets in IBD.
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BibTeX
@article{songelsanchis2026mycobiome,
title = {{Gut mycobiome dysbiosis in inflammatory bowel disease: a systematic review and meta-analysis}},
author = {Bruno Songel-Sanchis and Jesús Cosín-Roger},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1960101},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1960101/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Gut mycobiome dysbiosis in inflammatory bowel disease: a systematic review and meta-analysis
AU - Bruno Songel-Sanchis
AU - Jesús Cosín-Roger
PY - 2026
DA - 2026/10/15
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1960101
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1960101/full
AB - Background: The intestinal mycobiome is increasingly recognized as an important component of host–microbiota interactions in inflammatory bowel disease (IBD), yet its contribution to intestinal immune dysregulation remains incompletely characterized. We aimed to characterize alterations in the intestinal mycobiome in patients with inflammatory bowel disease, including Crohn’s disease and ulcerative colitis, compared with individuals without IBD, focusing on fungal diversity, taxonomic composition, and relative abundance, as well as their potential associations with disease phenotype and inflammatory activity. Methods: A systematic review and meta-analysis was conducted according to PRISMA 2020 guidelines. PubMed/MEDLINE, Embase, and Cochrane Central Register of Controlled Trials were systematically searched from inception to March 2026, with no language or publication-date restrictions. The review was not prospectively registered. Human studies assessing gut fungal communities by internal transcribed spacer (ITS)-based sequencing or shotgun metagenomics were eligible. Alpha and beta diversity, taxonomic composition, and clinically relevant fungal alterations were extracted. Study quality was assessed independently by two reviewers using the Newcastle–Ottawa Scale (NOS), and quantitative analyses were performed using standardized effect estimates and pooled prevalence. Results: Twenty-eight studies were included in the qualitative and quantitative synthesis. CD was consistently associated with reduced fungal alpha diversity compared with healthy controls, with a pooled weighted mean difference in Shannon diversity of −0.84 (p<0.001), whereas the reduction in UC was more modest (−0.31, p=0.04). Fungal beta diversity consistently differed between IBD and healthy controls. Expansion of Candida spp. was the most reproducible taxonomic alteration, occurring in 82.1% of analyzed cohorts, while depletion of Saccharomyces cerevisiae was reported in 71.4%. Malassezia enrichment was also associated with mucosal inflammation and CARD9-related immune responses. Cross-kingdom interactions involving Candida , Escherichia coli , and Serratia marcescens further highlighted potential fungal–bacterial mechanisms underlying persistent inflammation. Persistent fungal dysbiosis despite clinical remission supported the concept of a “mycobiotic scar.” Conclusion: IBD is characterized by substantial disruption of the intestinal mycobiome, particularly in CD, with reduced fungal diversity, expansion of potentially pathogenic Candida spp., and depletion of protective fungal taxa. These alterations may contribute to immune dysregulation and therapeutic refractoriness and support the mycobiome as a potential source of biomarkers and therapeutic targets in IBD.
SN - 1664-3224
ER -