Microbial genomic analysis reveals the essential role of inflammation in bacteria-induced colorectal cancer

Janelle C. Arthur, Raad Z. Gharaibeh, Marcus Mühlbauer, Ernesto Perez-Chanona, Joshua M. Uronis, Jonathan McCafferty, Anthony A. Fodor () and Christian Jobin ()
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Janelle C. Arthur: University of North Carolina at Chapel Hill
Raad Z. Gharaibeh: University of North Carolina at Charlotte
Marcus Mühlbauer: University of North Carolina at Chapel Hill
Ernesto Perez-Chanona: University of North Carolina at Chapel Hill
Joshua M. Uronis: University of North Carolina at Chapel Hill
Jonathan McCafferty: University of North Carolina at Charlotte
Anthony A. Fodor: University of North Carolina at Charlotte
Christian Jobin: University of Florida

Nature Communications, 2014, vol. 5, issue 1, 1-11

Abstract: Abstract Enterobacteria, especially Escherichia coli, are abundant in patients with inflammatory bowel disease or colorectal cancer (CRC). However, it is unclear whether cancer is promoted by inflammation-induced expansion of E. coli and/or changes in expression of specific microbial genes. Here we use longitudinal (2, 12 and 20 weeks) 16S rRNA sequencing of luminal microbiota from ex-germ-free mice to show that inflamed Il10−/− mice maintain a higher abundance of Enterobacteriaceae than healthy wild-type mice. Experiments with mono-colonized Il10−/− mice reveal that host inflammation is necessary for E. coli cancer-promoting activity. RNA-sequence analysis indicates significant changes in E. coli gene catalogue in Il10−/− mice, with changes mostly driven by adaptation to the intestinal environment. Expression of specific genes present in the tumour-promoting E. coli pks island are modulated by inflammation/CRC development. Thus, progression of inflammation in Il10−/− mice supports Enterobacteriaceae and alters a small subset of microbial genes important for tumour development.

Date: 2014
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DOI: 10.1038/ncomms5724

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