.Oxalobacter formigenes does not Alter slc26a6 Protein Abundance in the Large Intestine of C57BL/6 Mice

Hyperoxaluria is a major risk factor for kidney stone disease, and there is no pharmaceutical treatment available (8-13, 15, 16). In 1980, an anaerobic bacterium called Oxalobacter formigenes was isolated from rumen contents that had sole substrate specificity for oxalate, and later it was isolated from both human and numerous other animal feces (1, 2). Subsequent studies demonstrated that the lack of intestinal Oxalobacter sp.activity was a potential risk factor in kidney stone disease (8-13, 15, 16). It was found that stone forming patients who were Oxalobacter-negative had significantly higher urinary oxalate excretion (8-13, 15, 16), and recurrent kidney stone episodes in stone-forming patients appeared to correlate with the lack of Oxalobacter colonization within the intestinal tract (8-13, 15, 16). In 2002, a study showed that a single oral dose of Oxalobacter reduced the urinary oxalate in four human subjects following an oxalate load (9). Hoppe et al. also reported results of sizeable but transient reductions in urinary oxalate excretion when small studies of pH patients were administered Oxalobacter in the form of a paste/capsule (7). In animal studies, Oxalobacter has been found in the feces of various wild animals, but it is generally not found in laboratory rats or mice (1). When animals were exposed to increasing amounts of dietary oxalate, such animals showed increased rates of oxalate degradation, which suggests that oxalate tolerance can be developed in animals, and intestinal absorption can be reduced by robust Oxalobacter activity (5). Also, when rats were given dietary supplementation of oxalate, orally administering whole cells or oxalate-degrading enzymes from Oxalobacter reduced urinary oxalate excretion (5). The PAT-1 protein is considered to be one of the primary candidates involved in intestinal oxalate transport. This transport protein is located on the apical membrane in the epithelial cells and mediates secretion of oxalate in mouse intestines (4).The goal of the present study was to determine whether the Oxalobacter-induced changes in oxalate transport (5) could be correlated with changes in the abundance of PAT-1 in the mouse large intestine.