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Background. Ulcerative Colitis (UC) is a frequent type of Inflammatory Bowel Disease, characterized by periods of remission and exacerbation. Gut dysbiosis may influence pathophysiology and clinical response in UC. The purpose of this study was to evaluate whether gut microbiota is related to the active and remission phases of UC compared to healthy subjects. Results. Cross-sectional study. Fecal samples from 18 patients with UC (clinically characterized as active (n=9), remission (n=9)) and 15 healthy subjects were collected. After fecal DNA extraction, the 16S rRNA gene was amplified and sequenced (Illumina MiSeq platform), operational taxonomic units were analyzed with the QIIME (Quantitative Insights Into Microbial Ecology) software. Alpha and beta diversities were compared between clinical settings, as well as the relation between most frequent genus with UC severity indicators. Gut microbiota composition revealed higher abundance of the phyla Proteobacteria and Fusobacteria in active UC, as compared with remission UC and healthy subjects. Likewise, marked abundance of the genus Bilophila and Fusobacteria were present in active UC, as compared with the other groups, whereas higher abundance of Faecalibacterium characterized both remission UC and healthy subjects. Microbial community’s richness and diversity in active UC were significantly different from the other groups. Relative abundance of Fecalibacterium and Roseburia showed higher correlation with fecal calprotectin, while relative abundance of Bilophila and Fusobacterium showed AUCs (Area under the curve) 0.917 and 0.988 for active vs remission UC, respectively. Conclusion. Gut dysbiosis is related to clinically relevant phases of UC and healthy controls. Particularly, Fecalibacterium, Roseburia, Bilophila, and Fusobacterium were identified as genus highly related with clinical phases of UC.

La enfermedad inflamatoria intestinal, originada principalmente por trastornos intestinales como colitis ulcerativa y enfermedad de Crohn, involucra una desregulación de la respuesta inmunitaria por efecto de la microbiota intestinal y efectos inflamatorios. Es mediante la activación y la proliferación de monocitos y macrófagos, así como por las células dendríticas, que se induce la liberación de citocinas: interleucina IL-1β, IL-1βA, IL-4, IL-6, IL-8, factor de necrosis tumoral alfa (TNF-α), IL-12, IL-17 e IL-23, promoviendo la activación de células NK y deteniendo la proliferación de células Treg y la liberación de IL-10 como citocina reguladora. Actualmente se han desarrollado moléculas inhibidoras de esta respuesta inflamatoria mediante anticuerpos que bloquean las señales inducidas por estas citocinas, o el receptor de superficie, entre ellos los anti-TNF, un inhibidor de IL-12/IL-23 (ustekinumab) y los mediadores de las JAK cinasas (tofacitinib), que han demostrado su eficacia, mostrando respuestas clínicas y tasas de remisión de la enfermedad de manera significativa en ensayos clínicos controlados comparados con tratamientos convencionales o con placebo.