Possible trigger found

Sometimes it can be difficult to interpret press releases to decide whether they're really announcing something revolutionary. From the European Molecular Biology Laboratory, and published in Nature, is such a case.

Our gut is home to an enormous number of bacteria, which live in harmony with us and help in food digestion. If they penetrate the wall of the intestine, however, these bacteria can become harmful and cause diseases. This is why a thin, continuous layer of interconnected cells, called an epithelium, lines the intestinal surface creating a barrier that prevents bacteria from crossing that border. The mechanisms that control the integrity of the epithelium and contribute to maintaining a healthy gut have remained unknown.

Arianna Nenci from the group of Manolis Pasparakis at the University of Cologne and Christoph Becker, a member of Markus Neurath's group in Mainz, investigated the role of NF-κB, a signaling molecule that helps cells cope with stress, in the intestinal epithelium. Using sophisticated genetic methods, they generated a mouse model that does not express NEMO, a protein needed to activate NF-κB, in intestinal epithelial cells. As a result, these mice developed severe chronic intestinal inflammation very similar to Colitis in humans.

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The finding that defective NF-κB signaling in the gut epithelium initiates the outbreak of inflammation in the intestine provides a new paradigm for the pathogenesis of inflammatory bowel disease. Since the immune systems of mice and humans are very similar, the insights gained through the mouse model are steps towards a better understanding of the mechanisms causing human inflammatory bowel diseases and may pave the way for novel therapeutic approaches.

So, while the researchers managed to causes Crohn's-like symptoms in mice, the press-release does not elaborate on why they conclude that their method of causing these symptoms is of relevance. However, from the abstract of the Nature article, it is obvious that there is indeed more substantial evidence available to those with access to the full article.