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Genomic association and further characterisation of faecal immunoglobulin A deficiency in German Shepherd dogs
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AbstractBackgroundImmunoglobulin A (IgA) deficiency, chronic enteropathies and exocrine pancreatic insufficiency (EPI) have a high prevalence in German Shepherd dogs (GSD). This prospective study determined the prevalence of faecal IgA deficiency (IgAD) in GSD and investigated several candidate genes and the canine genome for a region or locus co‐segregating with IgAD in GSD. Faecal IgA concentrations were quantified and genomic DNA was extracted from 8 GSD with an undetectable faecal IgA (classified as IgAD) and 80 non‐IgAD GSD. The canine minimal screening set II microsatellite markers were genotyped, with evidence of an association atp < 1.0 × 10−3. Faecal IgA concentrations were also tested for an association with patient clinical and biochemical variables.ResultsAllele frequencies observed using the candidate gene approach were not associated with faecal IgAD in GSD. In the genome‐wide association study (GWAS), the microsatellite marker FH2361 on canine chromosome 33 approached statistical significance for a link with IgAD in GSD (p = 1.2 × 10−3). A subsequent GWAS in 11 GSD with EPI and 80 control GSD revealed a significant association between EPI and FH2361 (p = 8.2 × 10−4).ConclusionsThe lack of an association with the phenotype of faecal IgAD in GSD using the candidate gene approach and GWAS might suggests that faecal IgAD in GSD is a relative or transient state of deficiency. However, the prevalence of faecal IgAD in GSD appears to be low (<3%). The relationship between faecal IgAD, EPI and loci close to FH2361 on canine chromosome 33 in GSD warrants further investigation.
Title: Genomic association and further characterisation of faecal immunoglobulin A deficiency in German Shepherd dogs
Description:
AbstractBackgroundImmunoglobulin A (IgA) deficiency, chronic enteropathies and exocrine pancreatic insufficiency (EPI) have a high prevalence in German Shepherd dogs (GSD).
This prospective study determined the prevalence of faecal IgA deficiency (IgAD) in GSD and investigated several candidate genes and the canine genome for a region or locus co‐segregating with IgAD in GSD.
Faecal IgA concentrations were quantified and genomic DNA was extracted from 8 GSD with an undetectable faecal IgA (classified as IgAD) and 80 non‐IgAD GSD.
The canine minimal screening set II microsatellite markers were genotyped, with evidence of an association atp < 1.
0 × 10−3.
Faecal IgA concentrations were also tested for an association with patient clinical and biochemical variables.
ResultsAllele frequencies observed using the candidate gene approach were not associated with faecal IgAD in GSD.
In the genome‐wide association study (GWAS), the microsatellite marker FH2361 on canine chromosome 33 approached statistical significance for a link with IgAD in GSD (p = 1.
2 × 10−3).
A subsequent GWAS in 11 GSD with EPI and 80 control GSD revealed a significant association between EPI and FH2361 (p = 8.
2 × 10−4).
ConclusionsThe lack of an association with the phenotype of faecal IgAD in GSD using the candidate gene approach and GWAS might suggests that faecal IgAD in GSD is a relative or transient state of deficiency.
However, the prevalence of faecal IgAD in GSD appears to be low (<3%).
The relationship between faecal IgAD, EPI and loci close to FH2361 on canine chromosome 33 in GSD warrants further investigation.
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