N-glycolylneuraminic acid (Neu5Gc) is synthesized from its N-acetyl precursor (Neu5Ac) by cytidine-5′-monophospho-N acetylneuraminic acid hydroxylase (CMAH). Absent in humans and ferrets, it is polymorphic in dogs. Loss of the CMAH gene generate a change in the structural profile of glycans of all tissues inducing the production of antibodies against Neu5Gc-glycans.
Hypothesis/Objectives
Prolonged uptake of Neu5Gc by negative-CMAH dog through red meat and dairy products from +CMAH mammals leads to a progressive Neu5Gc-glycans incorporation in host’s tissue (xenosialization), particularly if the gut microbiota is altered in de-sialilating bacteria determining an inflammatory reaction (“Xenosialitis”).
Animals
For Immunohistochemistry, gastro-entero-colic biopsies from archive material belonging to European, Asian and American breeds were analyzed (35 dogs per group). Also the fecal microbiota of 2 cohorts (127 + 167) of healthy and enteropathic dogs was evaluated.
Methods
We choosed a polyclonal antibody (Creative Diagnostic, DMABH-C003) for Neu5GC expression. The distribution of desializing bacteria was performed using two different sequencing techniques for different regions of the 16S rRNA gene.
Results
Neu5Gc resulted mainly expressed in colon of dogs with enteropathy (p< 0.005) with no relation to breed. Greater prevalence of Clostridiales and Bactroidales was observed in enteropathic dogs.
Conclusions and clinical importance
Dysbiosis with increase Clostridiales and Bacteroidales could predispose to xenosialization and intestinal inflammation in negative-CMAH dogs, with a possible greater desializing activity compared to healthy dogs. Increased Neu5GC could cause greater uptake of xenosialoantigens by enteropathic dogs since Bifidobacteria, known for their cross-feeding of sialic acids activity, did not differ between healthy and pathologic.
