Inflammatory bowel diseases (IBD) are associated with compositional and functional changes of the intestinal microbiota, but specific contributions of individual bacteria to chronic intestinal inflammation remain unclear. is a resident member of the human intestinal core microbiota that has been linked to the pathogenesis of IBD and induces chronic colitis in susceptible monoassociated IL-10-deficient (IL-10) mice. In this study, we characterized the colitogenic activity of as part of a simplified human microbial consortium based on seven enteric bacterial strains (SIHUMI). RNA sequencing analysis of isolated from monoassociated wild type and IL-10 mice identified 408 genes including 14 genes of the ethanolamine utilization () locus that were significantly up-regulated in response to inflammation. Despite considerable up-regulation of genes, deletion of ethanolamine utilization (Δ) had no impact on colitogenic activity in monoassociated IL-10 mice. However, replacement of the wild type bacteria by a Δ mutant in SIHUMI-colonized IL-10 mice resulted in exacerbated colitis, suggesting protective functions of ethanolamine utilization in complex bacterial communities. To better understand gene response in the presence of other microbes, we purified wild type cells from the colon content of SIHUMI-colonized wild type and IL-10 mice using immuno-magnetic separation and performed RNA sequencing. Transcriptional profiling revealed that the bacterial environment reprograms gene expression in response to inflammation, with the majority of differentially expressed genes not being shared between monocolonized and SIHUMI conditions. While in monoassociation a general bacterial stress response could be observed, expression of genes in SIHUMI-colonized mice was characterized by up-regulation of genes involved in growth and replication. Interestingly, in mice colonized with SIHUMI lacking enhanced inflammation was observed in comparison to SIHUMI-colonized mice, supporting the hypothesis that ethanolamine metabolism protects against colitis in complex consortia. In conclusion, this study demonstrates that complex bacterial consortia interactions reprogram the gene expression profile and colitogenic activity of the opportunistic pathogen toward a protective function.