(RxWiki News) Trillions of bacteria - that's right trillions with a "t" - are found inside the lining of the colon. When inflammation enters the picture, that's when trouble can start. The bacteria and inflammation can team up and become a deadly duo.
Researchers are calling their discovery a "two-hit model" - in which inflammation helps E. Coli and other bacteria to produce DNA changes that then can become cancerous.
Colorectal cancer can be the result of this process.
"Ask your doctor how to reduce inflammation."
Cancer thrives with inflammation. In fact, inflammation fuels several cancers. That's why people with inflammatory bowel disease (IBD) have higher risks of colorectal cancer.
Janelle C. Arthur, PhD, of the Center for Gastrointestinal Biology and Disease at the University of North Carolina, and colleagues explored the inflammation/bacteria connection and process.
“Our research demonstrates that: inflammation alone is not sufficient to promote development of colorectal cancer, contrary to the current paradigm," said corresponding author, Christian Jobin, PhD, associate professor of medicine at the University of North Carolina School of Medicine.
"The presence of bacteria that can change DNA is essential. And the bacteria's cancer-inducing ability is required for the disease to develop," Dr. Jobin told dailyRx in an email.
In an animal study, researchers found mice that were engineered to have IBD had fewer types of gut bacteria and more E. coli than did normal mice.
So what the researchers think is that the inflammation helps these bacteria to grow. And the bacteria then starts the cancer by producing a DNA-altering substance called colibactin.
While this was an animal study, researchers believe that this process may also occur in humans.
They found that like the mice, patients with IBC and colorectal cancer also had fewer bacteria types and more E. Coli than people without these diseases.
The study was published August 16 in the journal Science.
This work was supported by funding from the National Institutes of Health, the American Institute for Cancer Research, University of North Carolina University Cancer Research Fund, NY Presbyterian/Weill Cornell Medical College, Crohn’s and Colitis foundation UK, the North West Cancer Research Fund UK and the Canadian Institutes of Health Research.
Several of the authors disclosed financial relationships with pharmaceutical companies and other commercial entities, including Atlantic, Proctor & Gamble, Abbott and GlaxoSmithKline, among others.
