Gut pathogens · 2026
Fungal abundance across flare and remission in ulcerative colitis patients.
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Herrera-deGuise Claudia, Varela Encarna, Sarrabayrouse Guillaume, Yáñez Francisca, Mayorga-Ayala Luis, Robles-Alonso Virginia, Céspedes-Martínez Elena, Serra-Ruiz Xavier, Lastiri Ernesto, Guarner Francisco, Borruel Sainz Natalia
Аннотация
BACKGROUND: Ulcerative colitis (UC) is associated with gut microbiota alterations, but the role of the fungal microbiota remains underexplored. We conducted a prospective study quantifying absolute bacterial and fungal abundance in faecal samples from UC patients with varying disease activity.
METHODS: We amplified the ITS2 sequence (fungi) and 16 S rRNA gene (bacteria) in three groups of patients: UC long remission (UClr); UC short remission (UCsr) and UC flare (UCfl). Two faecal samples from UClr and UCsr, and one sample from UCfl group (at flare-onset) were collected.
RESULTS: Eighty-seven patients were included: 29 UClr, 20 UCsr, and 38 UCfl. Across all patients, fungal ITS2 gene copies were markedly lower than bacterial 16 S rRNA copies (median 9.27E + 05 vs. 4.28E + 11 copies/g), with a fungal-to-bacterial ratio of 1:461,000. Fungal abundance was significantly higher in UCfl than in UClr (p = 0.0026), but not UCsr. The ITS2/16S ratio was also elevated in UCfl versus both remission groups (p < 0.01). Over time, fungal abundance showed greater variability than bacterial abundance, with a modest but significant decrease in the ITS2/16S ratio at 8 weeks (p = 0.029).
CONCLUSION: While bacterial loads remained stable across disease states, fungal abundance and the fungal-to-bacterial ratio were higher during UC flares. These findings describe an association between fungal dynamics and disease activity in UC and support further investigation of inter-kingdom microbial relationships in this context.
METHODS: We amplified the ITS2 sequence (fungi) and 16 S rRNA gene (bacteria) in three groups of patients: UC long remission (UClr); UC short remission (UCsr) and UC flare (UCfl). Two faecal samples from UClr and UCsr, and one sample from UCfl group (at flare-onset) were collected.
RESULTS: Eighty-seven patients were included: 29 UClr, 20 UCsr, and 38 UCfl. Across all patients, fungal ITS2 gene copies were markedly lower than bacterial 16 S rRNA copies (median 9.27E + 05 vs. 4.28E + 11 copies/g), with a fungal-to-bacterial ratio of 1:461,000. Fungal abundance was significantly higher in UCfl than in UClr (p = 0.0026), but not UCsr. The ITS2/16S ratio was also elevated in UCfl versus both remission groups (p < 0.01). Over time, fungal abundance showed greater variability than bacterial abundance, with a modest but significant decrease in the ITS2/16S ratio at 8 weeks (p = 0.029).
CONCLUSION: While bacterial loads remained stable across disease states, fungal abundance and the fungal-to-bacterial ratio were higher during UC flares. These findings describe an association between fungal dynamics and disease activity in UC and support further investigation of inter-kingdom microbial relationships in this context.