The study tracked a variety of genetic and chemical changes in the livers and colons of mice infected with Helicobacter hepaticus, a bacterium similar to Helicobacter pylori, which causes stomach ulcers and cancer in humans.
The findings could help researchers develop ways to predict the health consequences of chronic inflammation, and design drugs to halt such inflammation.
"If you understand the mechanism, then you can design interventions," says Peter Dedon. "For example, what if we develop ways to block or interrupt the toxic effects of the chronic inflammation?"
For the past 30 years, Steven Tannenbaum has led a group of MIT researchers dedicated to studying the link between chronic inflammation and cancer. Inflammation is the body's normal reaction to any kind of infection or damage, but when it goes on for too long, tissues can be damaged.
When the body's immune system detects pathogens or cell damage, it activates an influx of cells called macrophages and neutrophils. These cells' job is to engulf bacteria, dead cells and debris: proteins, nucleic acids and other molecules released by dead or damaged cells. As part of this process, the cells produce highly reactive chemicals that help degrade the bacteria.
"In doing this, in engulfing the bacteria and dumping these reactive chemicals on them, the chemicals also diffuse out into the tissue, and that is where the problem comes in," Dedon says.
If sustained over a long period, that inflammation can eventually lead to cancer. A recent study found that infections account for about 16 per cent of new cancer cases worldwide.
In the new study, the researchers analysed mice that were infected with H. hepaticus, which causes them to develop a condition similar to inflammatory bowel disease in humans. Over the course of 20 weeks, the mice developed chronic infections of the liver and colon, with some of the mice developing colon cancer.
MEDICA.de; Source: Massachusetts Institute of Technology (MIT)