Animal and human studies have provided compelling evidence that colonization of the intestine with Oxalobacter formigenes reduces urinary
oxalate excretion and lowers the risk of forming
calcium oxalate kidney stones. The mechanism providing protection appears to be related to the unique ability of O. formigenes to rely on
oxalate as a major source of
carbon and energy for growth. However, much is not known about the factors that influence colonization and host-bacterium interactions. We have colonized mice with O. formigenes OxCC13 and systematically investigated the impacts of diets with different levels of
calcium and
oxalate on O. formigenes intestinal densities and urinary and intestinal
oxalate levels. Measurement of intestinal
oxalate levels in mice colonized or not colonized with O. formigenes demonstrated the highly efficient degradation of soluble
oxalate by O. formigenes relative to other microbiota. The ratio of
calcium to
oxalate in diets was important in determining colonization densities and conditions where urinary
oxalate and fecal
oxalate excretion were modified, and the results were consistent with those from studies we have performed with colonized and noncolonized humans. The use of low-
oxalate purified diets showed that 80% of animals retained O. formigenes colonization after a 1-week dietary
oxalate deprivation. Animals not colonized with O. formigenes excreted two times more
oxalate in feces than they had ingested. This nondietary source of
oxalate may play an important role in the survival of O. formigenes during periods of dietary
oxalate deprivation. These studies suggest that the mouse will be a useful model to further characterize interactions between O. formigenes and the host and factors that impact colonization.