Investigators from Erasmus Medical Center, The Netherlands, uncovered a role for the protein Cd1d in regulating intestinal colonization by bacteria in mice. They report that the protein exerts its control through mechanisms that include the control of Paneth cell function.
Reporting in the Journal of Clinical Investigation in a paper called “Cd1d-dependent regulation of bacterial colonization in the intestine of mice,” the team analyzed Cd1d-sufficient and Cd1d-deficient mice. Under specific pathogen-free or germ-free conditions, they administered a number of species of bacteria like P. aeruginosa, E. coli, S. aureus, or L. gasseri.
Compared with Cd1d-sufficient mice, Cd1d-deficient mice exhibited increased colonization of the small intestine after these bacteria were administered into their stomachs, according to the researchers. In contrast, activation of Cd1d-restricted T cells (NKT cells) diminished intestinal colonization with the same bacterial strains.
The scientists also found differences in the composition of intestinal microbiota, including increased adherent bacteria in Cd1d-deficient mice under specific pathogen–free conditions. Germ-free Cd1d-deficient mice exhibited a defect in Paneth cell granule ultrastructure and ability to degranulate after bacterial colonization. In vitro, NKT cells were shown to induce the release of lysozyme from intestinal crypts.