Discordance between changes in the gut microbiota and pathogenicity in a mouse model of spontaneous colitis

Maria Elisa Perez-Muñoz, Kirk Bergstrom, Vincent Peng, Robert Schmaltz, Roberto Jimenez-Cardona, Nathan Marsteller, Sam McGee, Thomas Clavel, Ruth Ley, Jianxin Fu, Lijun Xia, Daniel A. Peterson

Research output: Contribution to journalArticlepeer-review

31 Scopus citations


Under conventional conditions, mice deficient in core 1-derived O-glycans (TM-IEC C1galt1-/-), which have a defective mucus layer, experienced spontaneous inflammation of the colon. Analysis of fecal bacterial populations by pyrosequencing of 16S rRNA gene showed that disease in conventional TM-IEC C1galt1-/- was associated with shifts in the microbiota manifested by increases in Lactobacillus and Clostridium species, and decreases in unclassified Ruminococcaceae and Lachnospiraceae. Under germ-free (GF) conditions, TM-IEC C1galt1-/- presented decreased goblet cells, but did not develop inflammation. Monoassociation of GF TM-IEC C1galt1-/- revealed that bacterial species differ significantly in their ability to induce inflammatory changes. Bacteroides thetaiotaomicron caused inflammation, while Lactobacillus johnsonii (enriched during colitis) did not. These observations demonstrate that not all microbiota shifts that correlate with disease contribute to pathogenesis.

Original languageEnglish (US)
JournalGut Microbes
Issue number3
StatePublished - Mar 24 2014
Externally publishedYes


  • Akkermasia muciniphila
  • Bacteroides sartorii
  • Bacteroides thetaiotaomicron
  • Clostridium
  • Core 1 O-glycans deficient mice
  • Dysbiosis
  • Gut microbiota
  • Lactobacillus johnsonii
  • Pyrosequencing
  • Spontaneous colitis

ASJC Scopus subject areas

  • Microbiology
  • Gastroenterology
  • Microbiology (medical)
  • Infectious Diseases


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