P666 Fruit consumption may protect against the development of intestinal inflammation via modification of microbial composition
L. Godny*1, N. Maharshak1, L. Yahav1, N. Fliss-Isakov2, U. Gophna3, H. Tulchinsky4, I. Dotan1
1Tel Aviv Sourasky Medical Centre, IBD Centre, Department of Gastroenterology and Liver Diseases, affiliated to the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel, 2Tel Aviv Sourasky Medical Centre, Department of Gastroenterology and Liver Diseases, affiliated to the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel, 3Tel Aviv University, Department of Molecular Microbiology and Biotechnology, George S. Wise Faculty of Life Sciences, Tel Aviv, Israel, 4Tel Aviv Sourasky Medical Centre, Proctology Unit, Department of Surgery, affiliated to the Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
Patients with ulcerative colitis (UC) undergoing proctocolectomy with ileal pouch-anal anastomosis commonly develop pouchitis. As pouchitis is inflammation developing in a previously normal small bowel. We hypothesise that it may represent the small intestinal inflammation characterising Crohn’s disease (CD). CD pathogenesis involves environmental factors. We thus asked whether diet and the microbiome had a role in pouch inflammation.
Patients recruited at the Comprehensive Pouch Clinic were prospectively followed-up. Pouch behaviour was determined clinically and defined as normal pouch (NP) or pouchitis. All patients completed food-frequency questionnaires (FFQs). Faecal samples were collected and analysed for microbial composition (16S rRNA gene pyrosequencing). Microbial diversity was calculated using Shannon diversity index. P- values were corrected for multiple comparisons using false discovery rate (FDR < 0.1).
In total, 172 pouch patients (89 [52%] females, with average age 44.9 ± 14 years and mean time since ileostomy closure 9.1 [range 0–30.4] years) were recruited. At the beginning of follow-up, 39 (22.6%) patients had NP. Within 1 year of follow-up, 5 (12.8%) of these developed pouchitis. Higher (> 1.45 servings/day), compared with lower fruit consumption was associated with significantly less development of pouchitis (3.8% vs 30.8%, respectively, log-rank test, p = 0.03). Faecal microbial analysis was performed in 81 patients (NP [n = 22], pouchitis [n = 53], and familial adenomatous polyposis [n = 7]). Fruit consumption correlated with microbial diversity (r = 0.37, p = 0.001), and with the abundance of several microbial groups. After adjustment for pouch behaviour and use of antibiotics, fruit consumption remained positively correlated with Faecalibacterium (r = 0.27, p = 0.01), Lachnospira (r = 0.31, p = 0.005), and 2 un-annotated genera from the Lachnospiraceae and Ruminococcaceae families (r = 0.24 p = 0.03; r = 0.28, p = 0.01, respectively). Significant decrease in fruit consumption was noticed in 10 patients who developed active disease over time (Δ = -1.4 ± 1.7 s/d, p = 0.02). Corresponding decrease in microbial diversity was noticed, as well (Δ = -0.6 ± 1.2, p = 0.17).
Fruit consumption of pouch patients significantly modified microbial composition, favouring expansion of Firmicutes, specifically Faecalibacterium, Lachnospiraceae, and Ruminococcaceae. Significant decrease in fruit consumption was associated with the development of active disease and with a decrease in microbial diversity. Thus, fruit consumption may be protective against intestinal inflammation, possibly by altering microbial composition. Therefore, dietary intervention may contribute to prevention of intestinal inflammation.