After an illness causes intestinal inflammation, a person may feel fully recovered. But the extracellular matrix of their intestines that acts like cellular tissue, may have an “inflammatory memory” for more than a year. This can derail normal recovery and increase the risk of chronic inflammatory diseases. The research was based on an animal model.
Inflammation is a natural defense reaction to infection or an injury. Once the problem has been handled, inflammation is supposed to subside on its own. It was thought that intestines healed after bouts of inflammation. This new research found that isn’t the case.
The extracellular matrix is a network of proteins and molecules that transmits signals between cells. Before this research, scientists didn’t realize it played such a large role in how the cells behave and recover. It was thought to be mechanical support.
Using a mouse model, scientists saw that, while the intestines appeared to recover a month after illness, the extracellular matrix “remembered.” The tissue didn’t regenerate correctly, and the shape of the intestines was distorted. The extracellular matrix itself was porous and nonrigid. The structural changes remained for 400 days.
This research could unlock our understanding of Crohn’s disease and ulcerative colitis. Scientists have never understood the cycle of inflammation remission and flare-ups seen in the two conditions. Understanding how inflammation harms the extracellular matrix may be the key.
Other recent research from Harvard found that gut inflammation could be linked to colorectal cancer years down the line. The study looked at the “epigenetic memory” of inflammation in the gut and found that it is likely a factor in colorectal tumors in a mouse model.
The researchers looked at the colon stem cells of mice and found that they have an epigenetic memory of inflammation more than 100 days after inflammation has stopped. The epigenetic change in regenerated tissue may make them more susceptible to malignant growths. In the model, when cancerous cells were introduced, the tissues with an epigenetic memory of inflammation grew larger tumors more quickly than tissues without previous inflammation.
As always, we caution that these studies were in animals, not people. Human research is needed before we can draw solid conclusions. And, if you are someone who has struggled with inflammation, you shouldn’t read this and take away the message that you are doomed. These studies may be key to learning how to prevent and treat chronic conditions better by understanding how inflammation plays a role.
