Intestinal inflammation targets cancer-inducing activity of the microbiota

Intestinal inflammation targets cancer-inducing activity of the microbiota

2012 October 5 | Janelle C. Arthur¹, Ernesto Perez-Chanona¹, Marcus Mühlbauer¹, Sarah Tomkovich¹, Joshua M. Uronis¹, Ting-Jia Fan¹, Barry J. Campbell², Turki Abujame³,⁴, Belgin Dogan⁵, Arlin B. Rogers⁶, Jonathan M. Rhodes², Alain Stintzi³, Kenneth W. Simpson⁵, Jonathan J. Hansen¹, Temitope O. Keku¹, Anthony A. Fodor⁷, and Christian Jobin¹
Inflammation promotes cancer by altering the intestinal microbiota, as shown in a study on colitis-associated colorectal cancer (CRC) in mice. The study found that inflammation modifies the gut microbiota in interleukin-10-deficient (Il10-/-) mice, increasing the abundance of certain bacteria, including Escherichia coli (E. coli), which can promote tumor development. The presence of a genotoxic island in E. coli, known as the polyketide synthase (pks) island, was linked to increased DNA damage and tumorigenesis. When E. coli was mono-associated with Il10-/- mice, it led to invasive carcinoma, while the absence of the pks island reduced tumor formation without affecting inflammation. The study also found that mucosa-associated E. coli with the pks island were present in a high percentage of inflammatory bowel disease (IBD) and CRC patients, suggesting a potential role in human CRC. The research highlights the interaction between inflammation and the microbiota in promoting CRC, with the pks island in E. coli playing a key role in DNA damage and tumorigenesis. The findings suggest that inflammation targets the microbiota, promoting the expansion of genotoxic bacteria that contribute to CRC. The study provides evidence that the presence of pks+ bacteria in the gut can enhance the carcinogenic potential of the microbiota in the context of chronic inflammation.Inflammation promotes cancer by altering the intestinal microbiota, as shown in a study on colitis-associated colorectal cancer (CRC) in mice. The study found that inflammation modifies the gut microbiota in interleukin-10-deficient (Il10-/-) mice, increasing the abundance of certain bacteria, including Escherichia coli (E. coli), which can promote tumor development. The presence of a genotoxic island in E. coli, known as the polyketide synthase (pks) island, was linked to increased DNA damage and tumorigenesis. When E. coli was mono-associated with Il10-/- mice, it led to invasive carcinoma, while the absence of the pks island reduced tumor formation without affecting inflammation. The study also found that mucosa-associated E. coli with the pks island were present in a high percentage of inflammatory bowel disease (IBD) and CRC patients, suggesting a potential role in human CRC. The research highlights the interaction between inflammation and the microbiota in promoting CRC, with the pks island in E. coli playing a key role in DNA damage and tumorigenesis. The findings suggest that inflammation targets the microbiota, promoting the expansion of genotoxic bacteria that contribute to CRC. The study provides evidence that the presence of pks+ bacteria in the gut can enhance the carcinogenic potential of the microbiota in the context of chronic inflammation.
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Understanding Intestinal Inflammation Targets Cancer-Inducing Activity of the Microbiota