Role of Intestinal Microbiota in Ulcerative Colitis

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Table 5: Animal studies used to demonstrate prebiotic effects in preventing colitis Reference (Osman et al., 2006) (Hoentjen et al., 2005) (Geier et al., 2007) (Lara‐Villoslada et al., 2006) Theoretical part (Cherbut et al., 2003) (Rodriguez‐ Cabezas et al., 2010) 26 (Rumi et al., 2004) 4. Modulation of the gut microbiota Key findings Compared with colitis control, the prebiotic Decreased severity of colonic damage Increased cecal and colonic lactobacilli and bifidobacteria Decreased IL‐1β Decreased neutrophile infiltration Compared with colitis control, the prebiotic Decreased severity of colonic damage Increased cecal and colonic lactobacilli and bifidobacteria Decreased IL‐1β Compared with colitis control, the prebiotic Increased neutrophile infiltration Did not result in greater reduction in colonic damage Compared with colitis control, the prebiotic Decreased severity of colonic damage Increased cecal and colonic lactobacilli and bifidobacteria Decreased neutrophile infiltration Compared with colitis control, the prebiotic Decreased severity of colonic damage Increased cecal and colonic lactobacilli and lactic acid bacteria Decreased neutrophile infiltration Compared with colitis control, the prebiotic Decreased severity of colonic damage Decreased neutrophile infiltration Increased colonic lactobacilli and bifidobacteria Did not affect the level of IL‐1β and TNF‐α Compared with colitis control, the prebiotic Decreased severity of colonic damage Decreased neutrophile infiltration Compared with colitis control, the prebiotic Decreased severity of colonic damage Decreased neutrophile infiltration Increased colonic lactobacilli and bifidobacteria Decreased colonic TNF‐α Compared with colitis control, the prebiotic Decreased severity of colonic damage Increased colonic TGF‐β Decreased colonic IL‐6 and IFN‐γ Compared with colitis control, the prebiotic Decreased severity of colonic damage Colitis inducer# DSS Study design animals Spraugue‐Dawley rats (n=6 in each group) Length of treatment * 14 days Substrate* OFI SPF HLA B27 transgenic rats (n=8 in each group) 7 weeks OFI DSS Spraugue‐Dawley rats (n=8 in each group) 14 days FOS TNBS Wistar rats (n=20 in each group) 1 month FOS TNBS Wistar rats (n=6 in each group) 14 days FOS TNBS Wistar rats (n=10 in each group) 14 days FOS DSS Wistar rats (n=6 in each group) 14 days Lactulose (Camuesco et al., 2005) TNBS Wistar rats (n=10 in each group) 3 weeks Lactulose (Kanauchi et al., 2008) CD4+CD45RB high T cells SCID mice (n=8 in each group) 9 weeks GBF (Lara‐Villostada et al., 2006) GMO 14 days Spraugue‐Dawley rats (n=10 in DSS each group) Decreased neutrophile infiltration *Oligofructose‐enriched inulin (OFI), fructo‐oligosaccharide (FOS), Germinated barley foodstuff (GBF), Oligosaccharides from goat milk (GMO) #Dextran sulfate sodium (DSS), pathogen‐free conditions (SPF), trinitrobenzene sulfonic acid (TNBS) Severe combined immunodeficiency (SCID)
Theoretical part 5. Production of prebiotics and novel prebiotic candidates 5. Production of prebiotics and novel prebiotic candidates Non‐digestible poly‐ and oligosaccharides of various types are found as natural components in fruit, vegetables, milk and honey (Crittenden and Playne, 1996). With the exception of soybean oligosaccharides (produced by direct extraction from soybean whey) and lactulose (produced by alkaline isomerisation of lactose), most prebiotic oligosaccharides are manufactured using enzymatic processes (Crittenden and Playne, 1996;Rastall, 2007). They are either synthesized from monosaccharides (such as lactose and sucrose) by transglycosylation reactions or produced by controlled hydrolysis of polysaccharides, including starch, inulin or xylan (Crittenden and Playne, 1996;Grizard and Barthomeuf, 1999). In this chapter, the production of the classified prebiotic oligosaccharide, FOS, will be described, as well as the production of novel prebiotic candidates derived from pectin. 5.1. Fructo-oligosaccharides FOS is found in several kinds of plants and vegetables such as banana, onion, asparagus roots, artichokes, shallot, and wheat (Sangeetha et al., 2005). They are industrially produced in two ways leading to different products: either from inulin (commercially recovered from chicory root and Jerusalem artichoke) by hydrolysis or from transfructosylation of sucrose (Grizard and Barthomeuf, 1999). In commercial inulin, both linear chains of α‐D‐glucopyranosyl‐[β‐D‐fructofuranosyl (linked 2→1)]n‐ 1‐D‐fructofuranoside and β‐D‐fructopyranosyl‐[β‐D‐fructofuranosyl (linked 2 →1)]n‐1‐D‐ fructofuranoside residues are included. The number (n) of β‐D‐fructofuranose units varies from two to more than seventy units (Roberfroid and Delzenne, 1998). The production of FOS from inulin is a result of partial enzymic hydrolysis using inulinase (2,1‐β‐D‐fructan fructanohydrolase (EC 3.2.1.7)). This enzyme is specific for inulin and catalyzes the breakdown of β‐D‐fructosidic linkages in inulin in an endo‐type manner. The majority of the hydrolysates (FOS: DP2–10; average DP5) are fructofuranosyl residues, but a low proportion terminates in glycosyl residues (Roberfroid and Delzenne, 1998;Grizard and Barthomeuf, 1999). The industrial production of FOS from sucrose uses mainly fructosyltransferase or β‐ fructofuranosidase from bacterial and fungal sources (Yun et al., 1997;Kim et al., 1998). FOS derived from sucrose all terminate in glucosyl residues, and are thus non‐reducing. Additionally, 27
Page 1: Role of Intestinal Microbiota in Ul
Page 4 and 5: Role of Intestinal Microbiota in Ul
Page 6 and 7: Preface Preface This thesis present
Page 8 and 9: Summary Summary The microbiota of t
Page 10 and 11: Dansk sammendrag Dansk sammendrag M
Page 12 and 13: Introduction and objectives Introdu
Page 14 and 15: List of Manuscripts Not included in
Page 16 and 17: List of contents List of Centents P
Page 18 and 19: List of Centents Methodology append
Page 21 and 22: 1. The intestinal environment Theor
Page 23 and 24: Theoretical part 5 1. The intestina
Page 25 and 26: 2. The colonic environment Theoreti
Page 27 and 28: Theoretical part 9 2. The colonic e
Page 29 and 30: Table 1: The presence of glycoside
Page 31 and 32: Theoretical part Figure 3: The colo
Page 33 and 34: 3. Inflammatory Bowel disease Theor
Page 35 and 36: Theoretical part 17 3. Inflammatory
Page 37 and 38: Theoretical part 19 4. Modulation o
Page 43: Table 4: Clinical trials on the pre
Page 47 and 48: Theoretical part 5. Production of p
Page 49 and 50: Theoretical part 5. Production of p
Page 51: Methodology part
Page 54 and 55: Methodology part 6. Methodology, co
Page 60 and 61: Introduction Methodology part 42 Pa
Page 62 and 63: Abstract Background Detailed knowle
Page 64 and 65: depending the level of disease acti
Page 66 and 67: in 1 x TAE at 60 °C for 16 h at 36
Page 68 and 69: Statistics PCA were generated by SA
Page 70 and 71: The PCA of the Gram‐positive bact
Page 72 and 73: layer of UC patients and found that
Page 74 and 75: Acknowledgements The authors thank
Page 76 and 77: Table 2 ‐ 16S rRNA gene and 16S
Page 78 and 79: 1. Firmicutes phylum 2. Bacteroidet
Page 80 and 81: Supplementary Figure S1. Dice clust
Page 82 and 83: Reference List 1. Ahmed S, Macfarla
Page 84 and 85: 32. Matsuki T, Watanabe K, Fujimoto
Page 87 and 88: Methodology part Paper 2 Fecal lact
Page 89 and 90: Fecal lactobacilli and bifidobacter
Page 91 and 92: Introduction The mucus layer lining
Page 93 and 94: 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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Journal of Agricultural and Food Ch
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Methodology part Paper 5 Paper 5 Ma
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Appl Microbiol Biotechnol (2011) 90
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Methodology part Paper 6 Tailored e
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Process Biochemistry 46 (2011) 1039
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Table 1 List of enzymes. Enzyme Sou
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J. Holck et al. / Process Biochemis
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Intensity 50 0 C1 175.05 J. Holck e
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J. Holck et al. / Process Biochemis
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[29] Bauer S, Vasu P, Persson S, Mo
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Methodology part 150
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Methodology part 152 Appendix 1 hor
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Appendix 3 Methodology part Appendi
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Methodology part 156 Appendix 3
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7. Discussion and perspectives Disc
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Discussion and conclusion 161 7. Di
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References References Abreu,M.T., V
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References Derrien,M., Vaughan,E.E.
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References Haarman,M. and Knol,J. (
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References Lantz,P.G., Matsson,M.,
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References Matsuki,T., Watanabe,K.,
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References Pullan,R.D., Thomas,G.A.
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References Tannock,G.W. (2010). Ana
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National Food Institute Technical U
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