BACKGROUND: Specific pathogen-free (SPF), but not germfree (GF), interleukin 
(IL)-2-deficient (IL-2-/-) mice develop inflammatory bowel disease (IBD) at 10 
to 15 weeks of age. Gnotobiotic IL-2-/- mice monocolonized with E. coli mpk 
develop IBD at 25 to 33 weeks of age but not B. vulgatus mpk, E. coli Nissle 
1917, or mice cocolonized with both E. coli mpk and B. vulgatus.
METHODS: To determine genes regulated by these commensal bacteria, host gene 
expression in the colon of 8-week-old IL-2-/- mice was compared by using 
microarrays and semiquantitative reverse-transcription polymerase chain 
reaction. Colonization with E. coli mpk/B. vulgatus or SPF microbiota altered 
the gene expression profile more profoundly than monocolonization with either B. 
vulgatus, E. coli mpk or E. coli Nissle indicating that the complexity of the 
gene expression pattern is influenced by the diversity of the microbiota.
RESULTS: A small but distinct group of genes could be defined which might be 
associated with colitis development. Thus, 8 week old E. coli mpk IL-2-/- mice 
rone to colitis compared to E. coli Nissle, B. vulgatus and E. coli mpk/B. 
vulgatus IL-2-/- mice displayed a lower expression of the anti-inflammatory 
RegIII family genes such as RegIII[gamma] and pancreatitis associated protein 
(PAP) and peroxisome proliferator-activated receptor-[gamma] regulated genes 
such as adipsin and adiponectin.
CONCLUSION: The increased expression of these genes in B. vulgatus colonized 
mice might be associated with prevention of E. coli mpk triggered colitis in E. 
coli mpkM/B. vulgatus IL-2-/- mice.