P677 Fungal abundance is related to inflammatory status in Ulcerative Colitis

Abstract

Background Fungi account for approximately 0.1% of the total microorganisms in the gut. Despite the vast body of literature on the bacterial component of the gut microbiota, little has been published on the fungal microbiota. Fungal-bacterial interactions may be significant in inflammatory bowel disease (IBD), with several lines of evidence linking fungi and IBD. Our study aimed to explore and compare the fungal and bacterial loads in fecal samples from different ulcerative colitis (UC) patients’ groups. Methods Using two qPCR systems to amplify the ITS2 sequence from fungi and the 16srRNA gene from bacteria, we characterized and compared fungal and bacterial loads in 3 groups: 1) UClr: UC patients in long-term remission (≥5 years of flare-free disease, clinical, endoscopic and histological remission at inclusion); 2) UCsr: UC patients in short-term remission (3 months in clinical remission at inclusion and previously more than one relapse/year); 3) UCfl: UC patients with active disease (CAI >4 at inclusion). We obtained two frozen fecal samples from all subjects, except for the UCfl group from which we obtained 1 sample at flare onset. Results were expressed in copies/g of feces. Results We included 87 UC patients, 29 in UClr, 20 in UCsr, and 38 in UCfl groups. Median age was 39 years, women comprised 52%. Fecal samples contained a significantly lower number of ITS2 gene copies (median 9.27E+05) than 16srRNA gene copies (median 4.28E+11). 16s rRNA gene copies were similar among the different groups with a median 3.88E+11 for UClr, median 5.29E+11 for UCsr, and median 4.315E+11 for UCfl patients (FDR p=0.65). In contrast, copies of ITS2 gene were increased in UCfl (median 1.95E+06) when compared to UClr (3.68E+04, FDR p=0.0036) but not significantly different to UCsr (5.24E+05 copies, FDR p=0.20). We analyzed the variation between samples over time; we compared the number of copies of ITS2 and 16s rRNA genes in fecal samples collected at two different time points: basal versus 8-weeks. We calculated overall fold changes that reflect stability over time. We found a trend for a more significant variation in the quantity of the ITS2 gene than the 16srRNA gene, but this was not significant. Analysis of the ITS2/16S rRNA ratio assessing the frequency of fungi compared to bacteria showed that this ratio was higher in UCfl (median 6.94E-06) when compared to UClr (median 2.63E-07, FDR p=0.0005) and UCsr patients (median 5.60E-07, FDR p=0.0072), there were no differences between UClr and UCsr patients. Conclusion Fungal abundance was increased in UC flare patients compared to UC patients in long remission, while there were no differences in bacterial abundance. This high number of fungi could be involved in the inflammatory response of UC patients.