Scientist - News - 09-04-2009:

Protein Cd1d mediates bacterial colonization
Beintema, Nienke

Researchers from the Erasmus Medical Center in Rotterdam, The Netherlands, have identified a protein that plays a role in regulating bacterial colonization of the small intestine in mice.

The small intestine contains much lower numbers of bacteria than the colon. Several factors contribute to this difference. One is the secretion of antibacterial compounds, such as lysozyme, by specific cells at the base of the small intestine, called Paneth cells. The mechanism of Paneth cell regulation is still largely unknown. An international group of researchers, led by Edward Nieuwenhuis at the Erasmus Medical Centre in Rotterdam and including scientists from Harvard and Tokyo, has discovered that the protein Cd1d plays a role in this pathway. The results appeared this week in the Journal of Clinical Investigation.

Assumption
Cd1d is known to play a role in pathogen defense. It is produced both in intestinal epithelial cells and in blood cells that play a role in the immune system. Cd1d stimulates these cells to produce antibacterial compounds. This led the researchers to speculate that the protein also plays a role in regulating the colonization of the small intestine by regulating the activity of Paneth cells. This assumption proved to be correct.

Pathway manipulation
Paneth cells of mice that lacked the gene coding for Cd1d showed a different structure and function than those of normal mice. If raised under germ-free conditions and then exposed to several strains of bacteria, these Cd1d-deficient mice showed a much more rapid intestinal colonization than controls. This was true both for harmless and for pathogenic bacteria. The researchers also found differences in the composition of intestinal microbiota between Cd1d-deficient mice and controls. They conclude that manipulation of the Cd1d pathway may offer a means to restrict mucosal exposure to invasive micro-organisms or commensals to which pathogenic responses occur, such as in inflammatory bowel disease.

More information:
Article in the Journal of Clinical Investigation
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