Role of Intestinal Microbiota in Ulcerative Colitis

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Discussion and conclusion 162 7. Discussion and perspectives The use of fecal samples to explore the colonic bacterial community in humans has been widely used, since these samples are easy to collect without invasive procedures compared to colonic biopsies (Takaishi et al., 2008;Sokol et al., 2009;Qin et al., 2010;Larsen et al., 2010). Nevertheless, the fecal microbiota may not be representative for the colonic mucosal microbiota, given that literature has revealed that the two microbiota communities differ from that of the others (Zoetendal et al., 2002;Eckburg et al., 2005;Turroni et al., 2009). In view of examining involvement of the intestinal microbiota in UC pathogenesis, the mucosal microbiota could be more relevant to study, due to their closer interaction with the epithelium (Derrien et al., 2011;Van den Abbeele et al., 2011b). However, owing to sampling restrictions, feces were analyzed in paper 1 to compare microbiota derived from healthy subjects and UC patients. 7.2. Modulation of the fecal microbial community from UC patients Bifidobacteria and lactobacilli are believed to play an important role in promoting intestinal health and species of both genera have shown to offer anti‐inflammatory effects by down‐regulation of pro‐inflammatory cytokines and induction of Treg cells (Hoarau et al., 2006;Peran et al., 2007;Ghadimi et al., 2010). A reduced level of lactobacilli and bifidobacteria could compromise the colon health and favor intestinal inflammation. Hence selective stimulation of lactic acid bacteria by prebiotics could be an approach to help decrease risk of flare‐ups in UC patients. In Paper 3, fermentation‐induced changes in fecal microbial communities obtained from either healthy subjects and UC patients in remission or relapse were investigated using arabino‐oligosaccharides (AOS; DP2‐10) derived from sugar beet pulp. The potential prebiotic properties of AOS was compared to FOS (classified prebiotic (Rastall, 2007)). Incubation with AOS and FOS gave rise to selective stimulation of bifidobacteria and lactobacilli in fecal microbial communities derived from UC patients. The ability of Bifidobacterium spp. and Lactobacillus spp. to utilize AOS or FOS and compete for substrate could be ascribed the presence of GH such as α‐L‐arabinofuranosidases (EC 3.2.1.55), and/or fructan β‐(2,1)‐fructosidase (EC 3.2.1.153) in species of these genera (http://www.cazy.org/ and http://www.uniprot.org/uniprot/, 2011‐10‐11). No human trials or in vivo studies have been reported examining the protective effect of AOS against colitis. However, the protective effect of FOS has been demonstrated in animals with induced colonic inflammation. The studies showed that consumption of FOS resulted in decreased severity of colonic damage and increased amount of colonic lactobacilli and bifidobacteria (Cherbut et al., 2003;Lara‐
Discussion and conclusion 163 7. Discussion and perspectives Villoslada et al., 2006;Rodriguez‐Cabezas et al., 2010). Additionally, Casellas et al. (2007) demonstrated that a mixture of FOS and inulin reduced disease activity in humans with UC after prebiotic consumption. The decreased levels of C. coccoides group, C. leptum subgroup and Desulfovibrio spp. after AOS and FOS incubation implied that these bacterial groups are not able to utilize AOS or FOS (paper 3). This is in agreement with results from database search of gene sequences that revealed that only few species of C. coccoides group, C. leptum subgroup and Desulfovibrio spp. contain α‐L‐ arabinofuranosidases (EC 3.2.1.55), and/or fructan β‐(2,1)‐fructosidase (EC 3.2.1.153) (http://www.cazy.org/, 2011‐10‐11). Though, it was expected based on cross‐feeding studies (Duncan et al., 2003;Belenguer et al., 2006;Marquet et al., 2009) that metabolites produced (e.g. acetate and lactate) during the fermentation of FOS and AOS could stimulate the growth of C. coccoides group, C. leptum subgroup and Desulfovibrio spp., however that was not observed in the study of paper 3. Hence, C. coccoides group, C. leptum subgroup and Desulfovibrio spp. are not able to compete in a fermentor community with AOS and FOS as primary carbohydrate sources. In addition, the inability of competing in the fermentor community with FOS and AOS was observed for Bacteroidetes. This was in line with previous communication, where species of Bacteroides have shown to be unable to utilize AOS (DP2‐5) and could only partly degrade FOS (Van Laere et al., 2000), even though genome sequencing has reveal that species of Bacteroides contain GH such as α‐L‐arabinofuranosidases (EC 3.2.1.55), arabinases (EC 3.2.1.99) and/or fructan β‐(2,1)‐ fructosidase (EC 3.2.1.153) (http://www.cazy.org/, 2011‐10‐22). Since feces is suggested to mainly consist of bacteria shed from the mucus or washed out from the lumen (Kurokawa et al., 2007;Booijink et al., 2007), both luminal and mucosal communities of lactobacilli and bifidobacteria may have been stimulated after incubation of AOS and FOS in Paper 3. Previous work by Van den Abbeele et al. (2011c) has shown that prebiotic candidates such as long‐chain arabinoxylans can stimulate bifidobacteria both in the mucus and lumen of humanized rats with Bifidobacterium longum being the most dominant Bifidobacterium species of both communities after prebiotic treatment. Collectively, the results from Paper 3 suggest that the positive effect already observed in human and animal trials using FOS may be applicable also for AOS. Hence presence and fermentation of AOS may help prevent pro‐inflammatory conditions and enhance resistance to colonization of
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Role of Intestinal Microbiota in Ul
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Role of Intestinal Microbiota in Ul
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Preface Preface This thesis present
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Summary Summary The microbiota of t
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Dansk sammendrag Dansk sammendrag M
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Introduction and objectives Introdu
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List of Manuscripts Not included in
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List of contents List of Centents P
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List of Centents Methodology append
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1. The intestinal environment Theor
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Theoretical part 5 1. The intestina
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2. The colonic environment Theoreti
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Theoretical part 9 2. The colonic e
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Table 1: The presence of glycoside
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Theoretical part Figure 3: The colo
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3. Inflammatory Bowel disease Theor
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Theoretical part 17 3. Inflammatory
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Theoretical part 19 4. Modulation o
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Table 4: Clinical trials on the pre
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Theoretical part 5. Production of p
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Methodology part
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Methodology part 6. Methodology, co
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Introduction Methodology part 42 Pa
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Abstract Background Detailed knowle
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depending the level of disease acti
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in 1 x TAE at 60 °C for 16 h at 36
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Statistics PCA were generated by SA
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The PCA of the Gram‐positive bact
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layer of UC patients and found that
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Acknowledgements The authors thank
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Table 2 ‐ 16S rRNA gene and 16S
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1. Firmicutes phylum 2. Bacteroidet
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Supplementary Figure S1. Dice clust
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Reference List 1. Ahmed S, Macfarla
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32. Matsuki T, Watanabe K, Fujimoto
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Methodology part Paper 2 Fecal lact
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Fecal lactobacilli and bifidobacter
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Introduction The mucus layer lining
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efore enrolment and there was no si
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(Bio‐Rad Labs, Hercules, Californ
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Microbial community analysis using
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difference from the luminal microbi
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that C. coccoides group and C. lept
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Table 1 ‐ 16S rRNA gene of phylum
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Table 2 ‐ Preference of bacterial
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Figure 1. A) Schematic overview of
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A. B. Figure 3. Principal component
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15. Fooks LJ, Gibson GR. (2002) In
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47. Ouwehand AC, Suomalainen T, Tol
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Methodology part Paper 3 Paper 3 In
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APPLIED AND ENVIRONMENTAL MICROBIOL
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8338 VIGSNÆS ET AL. APPL. ENVIRON.
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Methodology part Introduction The a
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