Ulcerative colitis has long been framed as a disorder of the gut’s bacterial residents, but a new prospective study suggests that the fungal side of the intestinal microbiome may be a far more active participant in the disease than previously appreciated. Researchers based primarily at Hospital Universitari Vall d’Hebron in Barcelona, working with collaborators in Paris and through the Spanish biomedical research network CIBEREHD, have found that fungal abundance in the gut rises significantly during disease flares in ulcerative colitis patients, even as bacterial loads remain essentially stable. The work, published open access in the journal Gut Pathogens, offers some of the most direct quantitative evidence to date that inter-kingdom shifts in the microbiome track with inflammatory disease activity.

The study set out to address a persistent gap in inflammatory bowel disease research. While alterations in gut bacteria have been catalogued extensively in ulcerative colitis, the fungal microbiota, often called the mycobiota, has remained underexplored, partly because fungi make up such a tiny fraction of the gut’s microbial census. To quantify this minority population rigorously, the team took an approach that many microbiome studies neglect: rather than reporting relative percentages of microbial groups, which can be misleading when the total microbial load changes, they measured absolute numbers of fungal and bacterial genetic material in faecal samples using quantitative polymerase chain reaction techniques.

Specifically, the researchers amplified the ITS2 sequence, a segment of DNA in the fungal ribosomal RNA gene cluster that serves as a standard barcode for fungi, and the 16S ribosomal RNA gene, the workhorse marker for bacteria. By measuring gene copies per gram of faeces, they could compare true abundance rather than shifting proportions. This matters because if total microbial load changes during inflammation, relative abundance data alone can suggest differences that do not reflect real changes in absolute numbers, or mask genuine ones.

The study enrolled eighty-seven patients with ulcerative colitis and divided them into three groups according to disease activity. Twenty-nine patients were in long-standing remission, a group designated UClr. Twenty were in short remission, designated UCsr, meaning their disease had quieted more recently. And thirty-eight were experiencing an active flare, with samples collected at the onset of the flare before treatment changes could confound the picture. Critically, patients in the long and short remission groups provided two faecal samples over time, while flare patients provided one at flare onset, allowing the team to examine how microbial loads fluctuate within individuals across different disease states.

The headline result is striking for its sheer arithmetic. Across all patients, fungal ITS2 gene copies were dramatically outnumbered by bacterial 16S copies, with a median of roughly 927,000 fungal gene copies per gram of faeces against approximately 428 billion bacterial copies. That yields a fungal-to-bacterial ratio of about one to 461,000, a vivid reminder that even a substantial expansion of the gut’s fungal population involves organisms that remain vanishingly rare compared with bacteria. Yet the small size of this population did not make it inert.

When the researchers compared across disease states, fungal abundance was significantly higher in patients during flares than in those in long remission, a difference that held up statistically with a p-value of 0.0026. The comparison with the short remission group did not reach significance, hinting that fungal dynamics may be tied to the timing and durability of disease quiescence rather than simply to the presence or absence of inflammation. Perhaps the most informative measure was the ratio of fungal to bacterial gene copies itself. Because bacterial numbers held steady across all groups, the ITS2 to 16S ratio effectively isolates the fungal signal. That ratio was significantly elevated in flare patients compared with both remission groups, with p-values below 0.01, suggesting a specific expansion of the fungal compartment during active disease rather than a general microbial shift.

The longitudinal data added a further layer. Among patients followed with repeated samples, fungal abundance proved considerably more variable over time than bacterial abundance, which remained stable. Within this fluctuation, the researchers documented a modest but statistically significant decrease in the fungal-to-bacterial ratio at eight weeks, with a p-value of 0.029, indicating that the mycobiota responds dynamically, and relatively quickly, to changes in the patient’s condition.

What these findings mean mechanistically remains an open question, and the authors are careful to frame the work as describing an association rather than proving causation. Several possibilities merit consideration. Fungal overgrowth could be a consequence of the intestinal environment during flares. Inflammation disrupts the mucosal barrier and changes the availability of oxygen and nutrients in the lumen, conditions that may favour fungal proliferation. Antibiotic use, altered mucus production and shifts in immune tone could also open ecological space for fungi. Alternatively, fungi could act as drivers of inflammation. The immune system recognises fungal cell wall components through pattern recognition receptors such as dectin-1 and the inflammasome, and increased fungal burden might amplify inflammatory signalling in a gut already primed for flare-ups.

The distinction between long and short remission groups introduces another intriguing dimension. The fact that flare patients differed significantly from those in long remission but not from those in short remission raises the possibility that the mycobiota settles into a more stable, restrained state only after remission has persisted for some time. If confirmed, this could suggest that fungal surveillance or antifungal interventions might be most relevant in the vulnerable early period after an episode of active disease, when the risk of relapse is highest.

The study’s methodological choices strengthen its conclusions. Absolute quantification is a deliberate corrective to the relative-abundance framework that dominates much microbiome sequencing work. In a fungal population numbering in the hundreds of thousands of copies per gram against a bacterial population in the hundreds of billions, subtle but real shifts in fungal load could easily disappear in percentage-based analyses or, conversely, appear exaggerated. By anchoring their measurements in absolute gene copy numbers, the Barcelona team has produced data that can be directly compared across future studies and, ultimately, translated into potential clinical markers.

The clinical implications are tantalising but preliminary. If elevated fungal burden proves to be a reliable accompaniment of flares, faecal ITS2 quantification could conceivably join the toolkit of biomarkers used to monitor ulcerative colitis, complementing established measures such as faecal calprotectin. More ambitiously, the findings invite speculation about antifungal or probiotic strategies that specifically target the mycobiota, or about dietary and pharmacological approaches that suppress fungal expansion during high-risk periods. But the authors themselves emphasise that association is not causation, and that the next step is deliberate investigation of inter-kingdom microbial relationships in inflammatory bowel disease, work that would determine whether fungi are passive beneficiaries of an inflamed gut or active contributors to the inflammatory cascade.

Ulcerative colitis affects millions of people worldwide, and its relapsing-remitting course means that predicting and preventing flares is one of the central challenges of patient care. The gut microbiome has been a fertile hunting ground for answers, but research has been overwhelmingly bacterial in focus. This study reframes the picture. In a disease of the intestinal lining, the rarest members of the microbial community, present at ratios of one in nearly half a million, may nonetheless carry information about disease state that the bacterial majority does not. The fungal microbiota, long a footnote in gut microbiome research, is now demonstrably part of the story, and its dynamics across the arc of disease activity deserve sustained scientific attention.

The research, conducted without external financial support and approved by the Clinical Research Ethics Committee of Hospital Universitari Vall d’Hebron, was published as an open access article, ensuring that patients, clinicians and researchers worldwide can examine the data in full. As the field moves from cataloguing who lives in the gut toward understanding how entire microbial ecosystems behave during disease, studies like this one make clear that ecosystems include more than bacteria, and that the smallest voices in the community may speak loudest when disease strikes.

Subject of Research: Fungal microbiota abundance in ulcerative colitis patients during flare and remission

Subject of Research: Biology

Article Title: Fungal abundance across flare and remission in ulcerative colitis patients

Article References: Herrera-deGuise, C., Varela, E., Sarrabayrouse, G., Yáñez, F., Mayorga-Ayala, L., Robles-Alonso, V., Céspedes-Martínez, E., Serra-Ruiz, X., Lastiri, E., Guarner, F., & Borruel Sainz, N. (2026). Fungal abundance across flare and remission in ulcerative colitis patients. Gut Pathogens, 18(1), Article 70. https://doi.org/10.1186/s13099-026-00846-0

Image Credits: AI Generated

DOI: 10.1186/s13099-026-00846-0

Keywords: Gut microbiota, Fungi, Ulcerative colitis, Inflammatory bowel disease, Mycobiota, ITS2, 16S rRNA, Fungal dysbiosis, Disease flare, Remission, Absolute abundance, Inter-kingdom microbial relationships

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Roger Howard. (September 8, 2026). Gut fungi shift between flares and remission in ulcerative colitis patients. Scienmag. https://scienmag.com/gut-fungi-shift-between-flares-and-remission-in-ulcerative-colitis-patients/

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