Phylogenetic analysis of dysbiosis in ulcerative colitis during remission

Typeset version

 

TY  - JOUR
  - Rajilic-Stojanovic, M.,Shanahan, F.,Guarner, F.,de Vos, W. M.
  - 2013
  - March
  - Inflammatory Bowel Diseases
  - Phylogenetic analysis of dysbiosis in ulcerative colitis during remission
  - Validated
  - ()
  - 19
  - 3
  - 481
  - 488
  - BACKGROUND: Presence of intestinal microbes is a prerequisite for the development of ulcerative colitis (UC), although deviation of the normal intestinal microbiota composition, dysbiosis, is presumably implicated in the etiology of UC. METHODS: The fecal microbiota of 30 UC samples obtained from 15 patients who were sampled twice and from 15 healthy control subjects originating from 2 geographic locations was analyzed using highly reproducible phylogenetic microarray that has the capacity for detection and quantification of more than 1000 intestinal bacteria in a wide dynamic range. RESULTS: The fecal microbiota composition is not significantly influenced by geographic location, age, or gender, but it differs significantly between the patients with UC and the control subjects (P = 0.0004). UC-associated microbiota is stable during remission and similar among all patients with UC. Significant reduction of bacterial diversity of members of the Clostridium cluster IV and significant reduction in the abundance of bacteria involved in butyrate and propionate metabolism, including Ruminococcus bromii et rel. Eubacterium rectale et rel., Roseburia sp., and Akkermansia sp. are markers of dysbiosis in UC. Increased abundance of (opportunistic) pathogens including Fusobacterium sp., Peptostreptococcus sp., Helicobacter sp., and Campylobacter sp. as well as Clostridium difficile were found to be associated with UC. CONCLUSIONS: Dysbiosis in UC is stable in time and shared between patients from different geographic locations. The microbial alterations offer a mechanistic insight into the pathogenesis of the disease.BACKGROUND: Presence of intestinal microbes is a prerequisite for the development of ulcerative colitis (UC), although deviation of the normal intestinal microbiota composition, dysbiosis, is presumably implicated in the etiology of UC. METHODS: The fecal microbiota of 30 UC samples obtained from 15 patients who were sampled twice and from 15 healthy control subjects originating from 2 geographic locations was analyzed using highly reproducible phylogenetic microarray that has the capacity for detection and quantification of more than 1000 intestinal bacteria in a wide dynamic range. RESULTS: The fecal microbiota composition is not significantly influenced by geographic location, age, or gender, but it differs significantly between the patients with UC and the control subjects (P = 0.0004). UC-associated microbiota is stable during remission and similar among all patients with UC. Significant reduction of bacterial diversity of members of the Clostridium cluster IV and significant reduction in the abundance of bacteria involved in butyrate and propionate metabolism, including Ruminococcus bromii et rel. Eubacterium rectale et rel., Roseburia sp., and Akkermansia sp. are markers of dysbiosis in UC. Increased abundance of (opportunistic) pathogens including Fusobacterium sp., Peptostreptococcus sp., Helicobacter sp., and Campylobacter sp. as well as Clostridium difficile were found to be associated with UC. CONCLUSIONS: Dysbiosis in UC is stable in time and shared between patients from different geographic locations. The microbial alterations offer a mechanistic insight into the pathogenesis of the disease.
  - 1078-09981078-0998
DA  - 2013/03
ER  - 
@article{V280546831,
   = {Rajilic-Stojanovic,  M. and Shanahan,  F. and Guarner,  F. and de Vos,  W. M. },
   = {2013},
   = {March},
   = {Inflammatory Bowel Diseases},
   = {Phylogenetic analysis of dysbiosis in ulcerative colitis during remission},
   = {Validated},
   = {()},
   = {19},
   = {3},
  pages = {481--488},
   = {{BACKGROUND: Presence of intestinal microbes is a prerequisite for the development of ulcerative colitis (UC), although deviation of the normal intestinal microbiota composition, dysbiosis, is presumably implicated in the etiology of UC. METHODS: The fecal microbiota of 30 UC samples obtained from 15 patients who were sampled twice and from 15 healthy control subjects originating from 2 geographic locations was analyzed using highly reproducible phylogenetic microarray that has the capacity for detection and quantification of more than 1000 intestinal bacteria in a wide dynamic range. RESULTS: The fecal microbiota composition is not significantly influenced by geographic location, age, or gender, but it differs significantly between the patients with UC and the control subjects (P = 0.0004). UC-associated microbiota is stable during remission and similar among all patients with UC. Significant reduction of bacterial diversity of members of the Clostridium cluster IV and significant reduction in the abundance of bacteria involved in butyrate and propionate metabolism, including Ruminococcus bromii et rel. Eubacterium rectale et rel., Roseburia sp., and Akkermansia sp. are markers of dysbiosis in UC. Increased abundance of (opportunistic) pathogens including Fusobacterium sp., Peptostreptococcus sp., Helicobacter sp., and Campylobacter sp. as well as Clostridium difficile were found to be associated with UC. CONCLUSIONS: Dysbiosis in UC is stable in time and shared between patients from different geographic locations. The microbial alterations offer a mechanistic insight into the pathogenesis of the disease.BACKGROUND: Presence of intestinal microbes is a prerequisite for the development of ulcerative colitis (UC), although deviation of the normal intestinal microbiota composition, dysbiosis, is presumably implicated in the etiology of UC. METHODS: The fecal microbiota of 30 UC samples obtained from 15 patients who were sampled twice and from 15 healthy control subjects originating from 2 geographic locations was analyzed using highly reproducible phylogenetic microarray that has the capacity for detection and quantification of more than 1000 intestinal bacteria in a wide dynamic range. RESULTS: The fecal microbiota composition is not significantly influenced by geographic location, age, or gender, but it differs significantly between the patients with UC and the control subjects (P = 0.0004). UC-associated microbiota is stable during remission and similar among all patients with UC. Significant reduction of bacterial diversity of members of the Clostridium cluster IV and significant reduction in the abundance of bacteria involved in butyrate and propionate metabolism, including Ruminococcus bromii et rel. Eubacterium rectale et rel., Roseburia sp., and Akkermansia sp. are markers of dysbiosis in UC. Increased abundance of (opportunistic) pathogens including Fusobacterium sp., Peptostreptococcus sp., Helicobacter sp., and Campylobacter sp. as well as Clostridium difficile were found to be associated with UC. CONCLUSIONS: Dysbiosis in UC is stable in time and shared between patients from different geographic locations. The microbial alterations offer a mechanistic insight into the pathogenesis of the disease.}},
  issn = {1078-09981078-0998},
  source = {IRIS}
}
AUTHORSRajilic-Stojanovic, M.,Shanahan, F.,Guarner, F.,de Vos, W. M.
YEAR2013
MONTHMarch
JOURNAL_CODEInflammatory Bowel Diseases
TITLEPhylogenetic analysis of dysbiosis in ulcerative colitis during remission
STATUSValidated
TIMES_CITED()
SEARCH_KEYWORD
VOLUME19
ISSUE3
START_PAGE481
END_PAGE488
ABSTRACTBACKGROUND: Presence of intestinal microbes is a prerequisite for the development of ulcerative colitis (UC), although deviation of the normal intestinal microbiota composition, dysbiosis, is presumably implicated in the etiology of UC. METHODS: The fecal microbiota of 30 UC samples obtained from 15 patients who were sampled twice and from 15 healthy control subjects originating from 2 geographic locations was analyzed using highly reproducible phylogenetic microarray that has the capacity for detection and quantification of more than 1000 intestinal bacteria in a wide dynamic range. RESULTS: The fecal microbiota composition is not significantly influenced by geographic location, age, or gender, but it differs significantly between the patients with UC and the control subjects (P = 0.0004). UC-associated microbiota is stable during remission and similar among all patients with UC. Significant reduction of bacterial diversity of members of the Clostridium cluster IV and significant reduction in the abundance of bacteria involved in butyrate and propionate metabolism, including Ruminococcus bromii et rel. Eubacterium rectale et rel., Roseburia sp., and Akkermansia sp. are markers of dysbiosis in UC. Increased abundance of (opportunistic) pathogens including Fusobacterium sp., Peptostreptococcus sp., Helicobacter sp., and Campylobacter sp. as well as Clostridium difficile were found to be associated with UC. CONCLUSIONS: Dysbiosis in UC is stable in time and shared between patients from different geographic locations. The microbial alterations offer a mechanistic insight into the pathogenesis of the disease.BACKGROUND: Presence of intestinal microbes is a prerequisite for the development of ulcerative colitis (UC), although deviation of the normal intestinal microbiota composition, dysbiosis, is presumably implicated in the etiology of UC. METHODS: The fecal microbiota of 30 UC samples obtained from 15 patients who were sampled twice and from 15 healthy control subjects originating from 2 geographic locations was analyzed using highly reproducible phylogenetic microarray that has the capacity for detection and quantification of more than 1000 intestinal bacteria in a wide dynamic range. RESULTS: The fecal microbiota composition is not significantly influenced by geographic location, age, or gender, but it differs significantly between the patients with UC and the control subjects (P = 0.0004). UC-associated microbiota is stable during remission and similar among all patients with UC. Significant reduction of bacterial diversity of members of the Clostridium cluster IV and significant reduction in the abundance of bacteria involved in butyrate and propionate metabolism, including Ruminococcus bromii et rel. Eubacterium rectale et rel., Roseburia sp., and Akkermansia sp. are markers of dysbiosis in UC. Increased abundance of (opportunistic) pathogens including Fusobacterium sp., Peptostreptococcus sp., Helicobacter sp., and Campylobacter sp. as well as Clostridium difficile were found to be associated with UC. CONCLUSIONS: Dysbiosis in UC is stable in time and shared between patients from different geographic locations. The microbial alterations offer a mechanistic insight into the pathogenesis of the disease.
PUBLISHER_LOCATION
ISBN_ISSN1078-09981078-0998
EDITION
URL
DOI_LINK
FUNDING_BODY
GRANT_DETAILS