EXPLAIN THE ORIGIN OF CROHN'S DISEASE

Explain the origin of Crohn's disease
25% of patients with Crohn's disease (inflammatory disease of the intestines) carry a mutation in the gene NOD2, the role of this mutation is not yet known. A Canadian stud led by Dr. Marcel Behr, of the Research Institute of the McGill University Health Centre (MUHC) partially lifts the veil on this mechanism. The results were published in the Journal of Experimental Medicine (reference below).

The NOD2 gene encodes a protein, a receptor in our immune system. NOD2 is an intracellular molecule capable of recognizing certain bacterial some special structures and thus act as an orchestrator of the immune response. In this study, researchers have shown that the NOD2 receptor recognizes preferentially a peptide called N-glycolyl-CDM, which is found only in a certain family of bacteria: mycobacteria. Thus, when a mycobacterium invades the human body, it provokes an immune response immediate and very strong through the receptor NOD2.

"Now that we know more about the normal role of NOD2, it is possible to hypothesize that the mutation prevents properly recognize mycobacteria,"

Dr. Behr said.

"Because mycobacteria are not recognized, they are not tackled effectively, and can infect the body so persistent."

The link between the presence of mycobacteria and Crohn's disease was already known to researchers, but whether the presence of bacteria was a cause or consequence of disease. This new discovery helps to involve susceptibility to Crohn's disease with the NOD2 mutation and the presence of mycobacteria: an association that brings together researchers from the mechanism of development of pathology.

Further research is needed to reach a satisfactory explanation. But they probably will open new therapeutic approaches to combat Crohn's disease.

Reference:
Article: Increased NOD2-mediated recognition of N-glycolyl muramyl dipeptide
Authors: Francois Coulombe, Maziar Divangahi Frederick Veyrier, Louis Leseleuc, James L. Gleason, Yibin Yang, Michelle A. Kelliher, Amit K. Pandey, Christopher M. Sassetti, Michael B. Reed and Marcel A. Behr
Journal Publication: Journal of Experimental Medicine

Source: EurekAlert
Credit: Institut Pasteur