Role of Intestinal Microbiota in Ulcerative Colitis

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Theoretical part 14 2. The colonic environment However, to avoid unnecessary detection of Gram‐positive commensal bacteria, IECs have developed special mechanisms to tolerate the continuous presence of LTA molecules originating from commensals by expressing TLR2 and co‐receptors at a limited level (Melmed et al., 2003;Lebeer et al., 2010). The same mechanism has been observed for TL4 on IECs, in which expression of TLR4 is down‐regulated to avoid hyper‐responsiveness to lipopolysaccharide (LPS) (Table 2) from commensal Gram‐negative bacteria (Abreu et al., 2001). In literature, immune regulatory effects of commensal bacteria through TLRs have been observed. As an example, Hoarau et al. (2006) demonstrated that the supernatant of B. breve could cause maturation of DCs through TLR2 pathway. This effect led to high levels of interleukin (IL)‐10 (inducer of regulatory T cells (Treg cells)) and low levels of IL‐12, in contrast to DCs stimulated with LPS. Another Bifidobacterium species, B. longum, has shown to attenuate Tumor Necrosis Factor‐ alfa (TNF‐α)‐induced Nuclear factor kappa B (NF‐κB) activation and NF‐κB‐mediated IL‐8 expression through TLR9 (Ghadimi et al., 2010). Finally, a study by Geuking et al. (2011) demonstrated that the colonization of mice with a completely benign commensal microbiota (altered Schaedler Flora) resulted in activation of colonic Treg cells in lamina propria through TLR signaling, which led to intestinal T cell homeostasis as reflected by the absence of T helper 1 cell or T helper 17 cell responses. Table 2: TLR recognition of Microbial Components Microbial Components Species TLR Usage References Triacyl lipopeptides Bacteria and mycobacteria TLR1 (Takeuchi et al., 2002) Peptidoglycan Gram‐positive bacteria TLR2 (Takeuchi et al., 1999;Schwandner et al., 1999) Fimbrillin Porphyromonas gingivalis TLR2/TLR4 (Davey et al., 2008) Polysaccharide A Bacteroides fragilis TLR2 (Round et al., 2011) Lipoarabinomannan Mycobacteria TLR2 (Means et al., 1999) Porins Neisseria TLR2 (Massari et al., 2002) Lipoteichoic acid Gram‐positive bacteria TLR2/TLR6 (Schwandner et al., 1999) Lipopolysaccharide Gram‐negative bacteria TLR4 (Poltorak et al., 1998) Flagellin Flagellated bacteria TLR5 (Hayashi et al., 2001) Diacyl lipopeptides Mycoplasma TLR6 (Takeuchi et al., 2001) CpG‐containing DNA Bacteria and mycobacteria TLR9 (Hemmi et al., 2000) Not determined Not determined TLR10 ‐ Not determined Uropathogenic bacteria TLR11 (Zhang et al., 2004)
3. Inflammatory Bowel disease Theoretical part 15 3. Inflammatory Bowel disease As described before, regulated interactions between commensal bacteria and host is important for colonic homeostasis, thus avoiding unnecessary reactions from the mucosal immune system. However, perturbation of this interaction can lead to colonic inflammation or worse diseases such as inflammatory bowel disease (IBD). This chapter will give a description of one of the IBDs, ulcerative colitis (UC), as well as elucidating some of the factors that may play a role for the pathogenesis of this disease. 3.1. Ulcerative colitis UC is an idiopathic IBD, which is characterized by chronic inflammation of the colonic mucosa. UC is usually associated with recurrent attacks and complete remission of symptoms in the interim. Generally, UC has a highly unpredictable clinical course characterized by one or more years with inactive disease and relapses, which typically last 2‐4 weeks provided that relevant treatment is given. The extent and severity of inflammation in the colon regions are variable. UC may be restricted to the distal colon and rectum (Proctitis, Proctosigmoiditis and Left‐sided colitis), while in its most extended form, the entire colon is involved (Pancolitis) (Figure 4) (Ardizzone, 2003;Kornbluth and Sachar, 2010). The classical symptoms of patients in relapse are diarrhea with passage of blood or mucus, or both, occasional abdominal cramping and pain as well as systemic symptoms of fever and weight loss in severe cases (Farrell and Peppercorn, 2002;Ardizzone, 2003). The medical treatments of UC are antibiotics, anti‐inflammatory drugs (e.g. mesalazine, olsalazine, sulfasalazine or corticosteroids), and/or immunosuppressive drugs (e.g. azathioprine, methotrexate or cyclosporine) (Kornbluth and Sachar, 2010). UC may affect any age group, although there is peak occurrence between ages 15 and 35. In Western Europe and USA, UC has an estimated prevalence of approximately 70 to 150 per 100.000 populations (Ardizzone, 2003;Kornbluth and Sachar, 2010).
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
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Page 29 and 30: Table 1: The presence of glycoside
Page 31: Theoretical part Figure 3: The colo
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Page 37 and 38: Theoretical part 19 4. Modulation o
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Page 62 and 63: Abstract Background Detailed knowle
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Page 68 and 69: Statistics PCA were generated by SA
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Page 74 and 75: Acknowledgements The authors thank
Page 76 and 77: Table 2 ‐ 16S rRNA gene and 16S
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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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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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Role of Intestinal Microbiota in Ulcerative Colitis

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