PRJNA353993
Genome sequence of Oxalobacter formigenes Human Strain HC-1
In the 80s, an anaerobic bacterium, with a substrate-specificity for oxalate, was isolated from rumen contents by Dr. M. Allison at Iowa State University (1). Later, when it was isolated from feces of humans and other animals, a new genus and species Oxalobacter formigenes, was established to include these microorganisms. Human patients forming oxalate kidney stones who are Oxalobacter-negative have significantly higher urinary oxalate excretion and recurrent kidney stone episodes appear to correlate with the lack of Oxalobacter colonization (2). Animal studies have shown that urinary oxalate excretion is significantly reduced when animals are colonized with Oxalobacter sp. compared to animals not colonized and this is partly due to a reduction in the intraluminal oxalate load available for absorption across the intestine because of this oxalate-degrading action (3, 4). Interestingly, however, studies in the Hatch lab have demonstrated that Oxalobacter has a dual action of deriving oxalate from systemic sources by initiating or enhancing intestinal oxalate secretion (i.e. enteric excretion) in addition to intraluminal degradation. This was initially substantiated in our laboratory using rats (4) and later in studies using mice (5,6). Remarkably, colonization of a mouse model of the genetic disease Primary Hyperoxaluria, type 1 (PH1) with Oxalobacter resulted in a normalization of both hyperoxaluria and hyperoxalemia exhibited in non-colonized counterparts (5). This was attributed to a physiological interaction between the bacteria and the enterocyte which induced active transmural oxalate excretion across the caecum and distal colon. Later studies confirmed that the human strain, HC-1, produced the same result in both the small and large intestine of wild type mice (6). This study was undertaken to determine and compare the genome sequence of HC-1 and OXCC13 which are both human strains of Oxalobacter formigenes isolated from two different individuals.1. Allison et al. (1985) Arch Microbiol, 141: 1-72. Hatch, M. and Freel, R.W. (2008) Sem in Neph, 28:143-1503. Sidhu et al. (1999) JASN. 10 Suppl 14: S334-404. Hatch et al. (2006) Kidney Int. 69: 691-6985. Hatch et al. (2011) Am J Physiol. 300 (3): 461-4696. Hatch, M. and Freel, R.W. (2013) Urolithiasis 41 (5):379-384