Towards explanation for Crohn's disease?
An innovative study at the Research Institute of the MUHC
has brought
us closer to an explanation for Crohn's disease
Twenty-five per cent of Crohn's disease patients have a mutation
in what is called the NOD2 gene, but it is not precisely known how
this mutation influences the disease. The latest study by Dr.
Marcel Behr, of the Research Institute of the MUHC and McGill
University, has provided new insight into how this might occur. The
study will be published on July 9th in the Journal of Experimental
Medicine.
When the NOD2 gene functions normally, it codes for a receptor that
will recognize invading bacteria and then trigger the immune
response. This study demonstrates that the NOD2 receptor
preferentially recognizes a peptide called N-glycolyl-MDP, which is
only found in a specific family of bacteria called mycobacteria.
When mycobacteria invade the human body, they cause an immediate
and very strong immune response via the NOD2 receptor.
"Now that we have a better understanding of the normal role of
NOD2, we think that a mutation in this gene prevents mycobacteria
from being properly recognized by the immune system," explained Dr.
Behr. "If mycobacteria are not recognized, the body cannot
effectively fight them off and then becomes persistently
infected."
Researchers were already aware of the relationship between
mycobacteria and Crohn's disease, but they did not know whether the
presence of bacteria was a cause or a consequence of the disease.
This new discovery associates the predisposition for Crohn's
disease with both the NOD2 mutation and the presence of
mycobacteria, but researchers must still determine the precise
combination of these factors to understand how the disease
develops.
More research is required to establish a complete explanation. From
this, it is expected that new therapeutic approaches that fight the
cause of Crohn's disease may be developed.
| Listen to the interview with Dr. Behr MP3 |
Dr. Marcel Behr
Dr. Marcel Behr is a researcher in the Infection and Immunity Axis
at the Research Institute of the MUHC and an Associate Professor of
Medicine and William Dawson Scholar of McGill University.
Funding
This study was funded by a grant from the Canadian Institutes of
Health Research (CIHR). The salaries of some researchers were
provided by the Fonds de la recherche en santé du Québec.
Partners
This article was co-authored by François Coulombe, Maziar Divanghi,
Frédéric Veyrier, Louis de Léséleuc, Dr. Michael B. Reed and Dr
Marcel Behr from the Research Institute of the MUHC; James L.
Gleason of McGill University; and Yibin Yang, Michelle A. Kelliher,
Amit K. Pandey, and Christopher M. Sassetti of the University of
Massachusetts Medical School.
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