The genetic composition of Oxalobacter formigenes and its relationship to colonization and calcium oxalate stone disease

Abstract

Oxalobacter formigenes is a unique intestinal organism that relies on oxalate degradation to meet most of its energy and carbon needs. A lack of colonization is a risk factor for calcium oxalate stone disease. Protection against calcium oxalate stone disease appears to be due to the oxalate degradation that occurs in the gut on low calcium diets with a possible further contribution from intestinal oxalate secretion. Much remains to be learned about how the organism establishes and maintains gut colonization and the precise mechanisms by which it modifies stone risk. The sequencing and annotation of the genomes of a Group 1 and a Group 2 strain of O. formigenes should provide the informatic tools required for the identification of the genes and pathways associated with colonization and survival. In this review we have identified genes that may be involved and where appropriate suggested how they may be important in calcium oxalate stone disease. Elaborating the functional roles of these genes should accelerate our understanding of the organism and clarify its role in preventing stone formation.

Figure 1

Oxalate catabolism and ATP synthesis in O. formigenes. Electrogenic oxalate2-:formate1- exchange forms the basis for sustaining a proton-motive force. Taken from Anantharam et. al., 1989 [3].

Figure 2

Number of fecal O. formigenes with changes in dietary oxalate. Daily calcium intake was 1000 mg. Real-time PCR was used to quantitate O. formigenes numbers. Reprinted from Jiang et. al. [34], with permission from Elsevier