A common bacterium – Escherichia coli (E. coli) – has been implicated as an inflammation trigger in people with genetic predisposition to Crohn’s disease.

French researchers recently reported this host-bacteria interaction pathway after studying and comparing cells in a laboratory from the colons of patients with Crohn’s disease and a control group. The researchers were able to demonstrate that infection with E. coli switches on an immune response that may lead to the inflammation that occurs in Crohn’s disease and other types of inflammatory bowel disease when the body’s own immune system revs up and cannot stop “protecting” itself.

As we have reported in previous issues of The Inside Tract®, while a genetic link has been found for Crohn’s disease, this represents only a small percentage of Crohn’s cases.

The investigators found that when E. coli infects the gut, levels of a molecule called MICA rise rapidly in the cells lining the intestine. The surge in MICA molecules – that seem to play an important role in the innate immune system – sets off a chain reaction, causing “killer” immune cells to release an immune-stimulating protein called gamma interferon.

Crohn’s patients had higher levels of MICA than controls, supporting the premise that E. coli could play a role in Crohn’s. This is a basic research study only and it is too early to tell whether testing for E. coli infection and treatment with antibiotics would be beneficial to Crohn’s patients.

The researchers also note that E. coli infection in the colon has already been associated with colorectal cancer.

First published in the Inside Tract® newsletter issue 130 – March/April 2002
V Tieng, C Le Bouguénec, L du Merle, et al. Binding of Escherichia coli adhesin AfaE to CD55 triggers cell-surface expression of the MHC class I-related molecule MICA. Proceedings of the National Academy of Sciences. 2002;99(5):2977-82