Role of Intestinal Microbiota in Ulcerative Colitis

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The PCA of the Gram‐positive bacteria showed no distinct clustering and no association of the UC patients group with particular bacterial genera was apparent (data not shown). Statistical analysis of the relative quantities of the fecal microbiota The relative quantities of the bacterial taxa obtained by qPCR (Table 3) revealed that the density of the Lactobacillus spp. was significantly lower in the UC patients in relapse than measured in the healthy controls (P < 0.05). The density of the butyrate‐producing bacterial group, Clostridium leptum subgroup was not significantly different between the three groups. However, there was a trend showing lower densities of Clostridium leptum subgroup in the UC patients in remission and relapse than in the healthy controls (P < 0.10). The overall density of the bacteria belonging to the Bacteroidetes phylum was significantly lower in the UC patients in remission than in the healthy controls (P < 0.05) and there was a trend of lower levels of Bacteroidetes in the UC patients in relapse than in the healthy controls (P < 0.10). Presence of Akk. muciniphila was detected only in three out of six fecal samples from UC patients in remission and three out of six fecal samples from UC patients in relapse, but in all the fecal samples (six out of six) of the healthy controls. Moreover, the average density of Akk. muciniphila in the three UC patients in relapse, in which it could be detected, was significantly lower than the average density of this species in the healthy controls (P < 0.05). No significant difference in Akk. muciniphila density was observed between the healthy controls and the UC patients in remission, in which it could be detected. The density of Bac. distasonis was not significantly different between the three groups. However, there was a trend showing lower densities in the UC patients in remission and relapse than in the healthy controls (P < 0.10). In the UC patients in relapse the density of Prevotella spp. was slightly but not significantly increased compared to the healthy controls (P < 0.10). The relative quantities of Bacteroides spp., Bac. uniformis, and Bac. thetaiotaomicron were somewhat higher in the UC patients in relapse compared to the healthy controls, although no significant difference could be measured (P > 0.10). Prevalence of selected Bifidobacterium species in fecal samples The prevalence of six selected Bifidobacterium species, commonly detected in human feces, is shown in Figure 3. Interestingly, Bifidobacterium bifidum was present in 2/6 healthy controls, and 10
in 4/6 UC patients in remission, but was not detectable in any of the 6 UC patients in relapse. In contrast, prevalences of Bifidobacterium adolescentis, Bifidobacterium catenulanum, and Bifidobacterium longum did not appear different between the three groups of samples. Bifidobacterium breve and Bifidobacterium angulatum were not detected in any of the 18 samples investigated. Discussion Since the intestinal bacterial microbiota is believed to represent an important environmental factor playing a pivotal role in the pathogenesis of UC, a thorough understanding of the intestinal microbial composition is of major importance for unravelling mechanisms responsible for flare‐ups of the disease. Cluster analysis of PCR‐DGGE‐based fingerprint and qPCR based PCA of the fecal communities revealed a different microbiota in UC patients compared to healthy controls, which is in good agreement with previous reports [15,41,51,52]. Differences in the DGGE‐based profiles could be explained mainly by variations within the genera Bacteroides, Prevotella and Alistipes (See additional file 2). Additionally, PCA of the qPCR data revealed that the difference between UC patients in relapse and healthy controls was most apparent within the targeted Gram‐negative bacteria and that Bacteroidetes, Akk. muciniphila, Desulfovibrio spp., and Bac. distasonis versus Bacteroides spp., Prevotella spp., Bac. thetaiotaomicron and Bac. uniformis accounted for the separation (Figure 2). These data imply that the composition and abundance of Gram‐negative bacteria, particularly those belonging to the Bacteroidetes phylum, may contribute to dysbiosis in colitis patients. A potent stimulator of inflammation from Gram‐negative bacteria is LPS. Hence, an unfavourable composition of the Gram‐negative bacteria may enhance abnormal LPS signaling and contribute to the sustained mucosal inflammation in UC patients. The mucin‐degrading bacterium Akk. muciniphila, which is a common member of the human microbiota has previously been reported as being involved in the pathogenesis of intestinal diseases [7,9,39]. In this study, a significantly lower density of Akk. muciniphila was found in UC patients in relapse than in the healthy control group. The reduced density of Akk. muciniphila could be a consequence of the reduced mucus layer in UC patients, since mucins constitute the primary carbon source of this species [53]. Pullan and coworkers [40] examined the colonic mucus 11
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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
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 and 44: Table 4: Clinical trials on the pre
Page 45 and 46: Theoretical part 5. Production of p
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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 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
Page 95 and 96: (Bio‐Rad Labs, Hercules, Californ
Page 97 and 98: Microbial community analysis using
Page 99 and 100: difference from the luminal microbi
Page 101 and 102: that C. coccoides group and C. lept
Page 103 and 104: Table 1 ‐ 16S rRNA gene of phylum
Page 105 and 106: Table 2 ‐ Preference of bacterial
Page 107 and 108: Figure 1. A) Schematic overview of
Page 109 and 110: A. B. Figure 3. Principal component
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Page 113 and 114: 47. Ouwehand AC, Suomalainen T, Tol
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Page 117 and 118: APPLIED AND ENVIRONMENTAL MICROBIOL
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8340 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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