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Assessment of Toll-like receptor 2, 4 and 9 SNP genotypes in canine sino-nasal aspergillosis

BACKGROUND: The exact aetiology of canine sino-nasal aspergillosis (SNA) is unknown. In man, dysfunction in innate immunity, particularly in the function of pattern recognition receptors, is implicated in the pathogenesis of inflammatory sino-nasal disease and in fungal diseases. Associations betwee...

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Autores principales: Mercier, Elise, Peters, Iain R, Farnir, Frédéric, Lavoué, Rachel, Day, Michael, Clercx, Cécile, Peeters, Dominique
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4143572/
https://www.ncbi.nlm.nih.gov/pubmed/25266752
http://dx.doi.org/10.1186/s12917-014-0187-6
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author Mercier, Elise
Peters, Iain R
Farnir, Frédéric
Lavoué, Rachel
Day, Michael
Clercx, Cécile
Peeters, Dominique
author_facet Mercier, Elise
Peters, Iain R
Farnir, Frédéric
Lavoué, Rachel
Day, Michael
Clercx, Cécile
Peeters, Dominique
author_sort Mercier, Elise
collection PubMed
description BACKGROUND: The exact aetiology of canine sino-nasal aspergillosis (SNA) is unknown. In man, dysfunction in innate immunity, particularly in the function of pattern recognition receptors, is implicated in the pathogenesis of inflammatory sino-nasal disease and in fungal diseases. Associations between single nucleotide polymorphisms (SNPs) in Toll-like receptors (TLRs) and these diseases have been identified. Similarly, in dogs SNPs in genes encoding TLRs may be important in the pathogenesis of SNA. The aims of the present study were (1) to identify the presence of non-synonymous SNPs in the coding regions of the TLR2, 4 and 9 genes in dogs suffering from SNA, and (2) to investigate the SNP genotypes in dogs with SNA compared with a control population. RESULTS: Direct sequencing of nine dogs of various breeds with SNA revealed two non-synonymous SNPs in the coding region of TLR2, eight in TLR4 and four in TLR9. These non-synonymous SNPs were further evaluated in a case-control study of affected Golden Retrievers, Labrador Retrievers, Rottweilers and Beaucerons. Genotyping was performed using a combination of allele-specific primers and hydrolysis probe assays in 31 dogs with SNA and 31controls. No significant difference in minor allele frequency was identified between these groups, for all studied SNPs, in any of the four breeds. CONCLUSIONS: These findings do not support a role for non-synonymous SNPs in the TLR 2, 4 and 9 coding regions in the pathogenesis of canine SNA, but do not exclude a role for innate immunity in the pathogenesis of the disease.
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spelling pubmed-41435722014-08-27 Assessment of Toll-like receptor 2, 4 and 9 SNP genotypes in canine sino-nasal aspergillosis Mercier, Elise Peters, Iain R Farnir, Frédéric Lavoué, Rachel Day, Michael Clercx, Cécile Peeters, Dominique BMC Vet Res Research Article BACKGROUND: The exact aetiology of canine sino-nasal aspergillosis (SNA) is unknown. In man, dysfunction in innate immunity, particularly in the function of pattern recognition receptors, is implicated in the pathogenesis of inflammatory sino-nasal disease and in fungal diseases. Associations between single nucleotide polymorphisms (SNPs) in Toll-like receptors (TLRs) and these diseases have been identified. Similarly, in dogs SNPs in genes encoding TLRs may be important in the pathogenesis of SNA. The aims of the present study were (1) to identify the presence of non-synonymous SNPs in the coding regions of the TLR2, 4 and 9 genes in dogs suffering from SNA, and (2) to investigate the SNP genotypes in dogs with SNA compared with a control population. RESULTS: Direct sequencing of nine dogs of various breeds with SNA revealed two non-synonymous SNPs in the coding region of TLR2, eight in TLR4 and four in TLR9. These non-synonymous SNPs were further evaluated in a case-control study of affected Golden Retrievers, Labrador Retrievers, Rottweilers and Beaucerons. Genotyping was performed using a combination of allele-specific primers and hydrolysis probe assays in 31 dogs with SNA and 31controls. No significant difference in minor allele frequency was identified between these groups, for all studied SNPs, in any of the four breeds. CONCLUSIONS: These findings do not support a role for non-synonymous SNPs in the TLR 2, 4 and 9 coding regions in the pathogenesis of canine SNA, but do not exclude a role for innate immunity in the pathogenesis of the disease. BioMed Central 2014-08-16 /pmc/articles/PMC4143572/ /pubmed/25266752 http://dx.doi.org/10.1186/s12917-014-0187-6 Text en Copyright © 2014 Mercier et al.; licensee BioMed Central Ltd http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Mercier, Elise
Peters, Iain R
Farnir, Frédéric
Lavoué, Rachel
Day, Michael
Clercx, Cécile
Peeters, Dominique
Assessment of Toll-like receptor 2, 4 and 9 SNP genotypes in canine sino-nasal aspergillosis
title Assessment of Toll-like receptor 2, 4 and 9 SNP genotypes in canine sino-nasal aspergillosis
title_full Assessment of Toll-like receptor 2, 4 and 9 SNP genotypes in canine sino-nasal aspergillosis
title_fullStr Assessment of Toll-like receptor 2, 4 and 9 SNP genotypes in canine sino-nasal aspergillosis
title_full_unstemmed Assessment of Toll-like receptor 2, 4 and 9 SNP genotypes in canine sino-nasal aspergillosis
title_short Assessment of Toll-like receptor 2, 4 and 9 SNP genotypes in canine sino-nasal aspergillosis
title_sort assessment of toll-like receptor 2, 4 and 9 snp genotypes in canine sino-nasal aspergillosis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4143572/
https://www.ncbi.nlm.nih.gov/pubmed/25266752
http://dx.doi.org/10.1186/s12917-014-0187-6
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