Inulin and fructo-oligosaccharides have divergent effects on colitis and commensal microbiota in HLA-B27 transgenic rats

Abstract

Modulation of intestinal microbiota by non-digestible carbohydrates may reduce inflammation in inflammatory bowel disease (IBD). The aim of the present study was to assess the effects of inulin and fructo-oligosaccharides (FOS) on intestinal microbiota and colitis in HLA-B27 transgenic rats, a well-validated rodent model for IBD. In this study, 4-week-old rats were fed 8 g/kg body weight inulin or FOS for 12 weeks, or not. Faeces were collected at 4 and 16 weeks of age; and caecal samples were collected at necropsy. The effects of inulin and FOS on chronic intestinal inflammation were assessed using a gross gut score, histology score and levels of mucosal IL-1b. Intestinal microbiota were characterised by quantitative PCR and denaturing gradient gel electrophoresis. Colitis was significantly reduced in all FOS-fed rats compared to the control diet, whereas inulin decreased chronic intestinal inflammation in only half the number of animals. Quantitative analysis of caecal microbiota demonstrated that inulin increased the numbers of total bacteria and the Bacteroides-PrevotellaPorphyromonas group, FOS increased bifidobacteria, and both fructans decreased Clostridium cluster XI. In the faecal samples, both inulin and FOS decreased total bacteria, Bacteroides-Prevotella-Porphyromonas group, and Clostridium clusters XI and XIVa. FOS increased Bifidobacterium spp., and mediated a decrease of gene copies of Enterobacteriaceae and Clostridium difficile toxin B in faeces. SCFA concentrations in the faecal and caecal samples were unaffected by the diets. In conclusion, FOS increased the abundance of Bifidobacterium spp., whereas both fructans reduced Clostridium cluster XI and C. difficile toxin gene expression, correlating with a reduction of chronic intestinal inflammation.

Fructooligosaccharides exert intestinal anti-inflammatory activity in the CD4+ CD62L+ T cell transfer model of colitis in C57BL/6J mice

“…In rats, FOS have been shown to exert colonic anti-inflammatory effects at doses ranging between 1 and 2 g day −1 , i.e. up to fourfold higher than the dose used in this study [11,[16][17][18], while at least some of the studies which failed to find therapeutic benefit employed lower doses [19]. In particular, a recent study showing beneficial effects of FOS in the HLA-B27 transgenic model of rat colitis used a dose of 8 g kg −1 , equivalent to roughly three times the dose used by us after correction for body surface [16].…”

“…Instead, a number of various models with different advantages and drawbacks are available. FOS have been shown to exert colitis protective actions in chemical models [11,[16][17][18], with some exceptions [19,20], and in HLA-B27 transgenic rat colitis [23]. The advantages of lymphocyte transfer colitis are its chronic course and the lymphocyte-driven pathology.…”

“…This has been evidenced by most [11,[16][17][18], but not all studies in animals [19,20]. Clinical studies range from small evidence of benefit to no effect [21,22], although in this scenario the experimental conditions are obviously less flexible, and therefore, it is possible to have an effective treatment fail, for instance, for an inadequate dose.…”

“…Clinical studies range from small evidence of benefit to no effect [21,22], although in this scenario the experimental conditions are obviously less flexible, and therefore, it is possible to have an effective treatment fail, for instance, for an inadequate dose. Animal studies have employed chemically induced models of colitis, namely trinitrobenzenesulfonic acid (TNBS) and dextran sulphate sodium (DSS), as well as other gene-targeted rodent models of spontaneous colitis, such as HLA-B27 transgenic rats [16,23]. There is no ideal animal model of IBD [24].…”

Probiotics and Cancer Prevention as a Part of the Healthy Microbiome

“…Some prebiotics can increase the abundance of probiotics (ex: Bifidobacterium spp). Other prebiotics decrease harmful organisms; for example, inulin and FOS to reduce Clostridium cluster XI and Clostridium difficile toxin gene expression and associated incidence of chronic intestinal inflammation in transgenic rats [8]. It should also be noted that possibly detrimental compounds may arise from microbial metabolism.…”