Paris, November 5, 2008
There are billions of bacteria in our intestine. These bacteria are not harmful, but help with digestion and also play a protective role by forming a barrier around the intestine, thus preserving it from attacks by pathogenic organisms. But, when their development ceases to be regulated, they can proliferate and become pathogenic themselves. The balance between these bacteria, known as commensals, and the immune system controlling them, is therefore essential. Changes in this balance can cause severe intestinal diseases, such as Crohn's disease, or other chronic inflammatory conditions with serious sequelae.
In an article published in Nature, Gerard Eberl and his Lymphoid Tissue Development Group at the Institut Pasteur (CNRS, URA1961) give a step-by-step description of a mechanism that maintains this subtle balance between intestinal commensal flora and the immune system. In particular, the researchers demonstrate how certain bacteria trigger an immune response leading to the formation of new lymphoid tissues responsible for modulating their development.
The scientists first show that an essential component of the bacterial wall, recognized by a protein in the epithelial cells of the intestine, triggers the first step of an immune chain reaction. This reaction leads to the formation of lymphoid tissues which, in turn, secrete immunoglobulins. It is these small molecules that control the bacterial flora on the surface of the intestine.
Above all, in cooperation with Ivo Gomperts Boneca and his Biology and Genetics of the Bacterial Cell Wall Group (Institut Pasteur/AVENIR Inserm Team), Gérard Eberl's team demonstrate that, once isolated, the bacterial cell wall component can alone induce this regulation mechanism. Thus, thanks to this molecule, researchers hope to contribute to the development of new forms of treatment against inflammatory diseases of the intestine and intestinal infections.
"Lymphoid tissue genesis induced by commensals through NOD1 regulates intestinal homeostasis", Nature, published on line on November 5, 2008.
Djahida Bouskra (1), Christophe Brézillon (2), Marion Bérard (3), Catherine Werts (4,6), Rosa Varona (5), Ivo Gomperts Boneca (4,6), Gérard Eberl (1).
(1) Institut Pasteur, Lymphoid Tissue Development Group, CNRS, URA1961.
(2) Institut Pasteur, Laboratory of Pathogenic Enteric Bacteria.
(3) Institut Pasteur, Central Animal Facility.
(4) Institut Pasteur, Biology and Genetics of the Bacterial Cell Wall Group.
(5) Department of Immunology and Oncology, Centro Nacional de Biotecnologia/CSIC, UAM Campus Cantoblanco, Madrid 28049, Spain.
(6) AVENIR Inserm Team “The role of peptidoglycan in bacterial cell physiology: morphology, resistance to b-lactams and host-microbe interactions”
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