Peer-reviewed veterinary case report
Gene expression differences in dogs with nasal aspergillosis
By Vanherberghen, Morgane et al.·Published in Veterinary microbiology·2012·Faculty of Veterinary Medicine·View original on PubMed →
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Original publication title: Analysis of gene expression in canine sino-nasal aspergillosis and idiopathic lymphoplasmacytic rhinitis: a transcriptomic analysis.
- Species:
- dog
Plain-English summary
A dog with nasal discharge was studied to understand two common causes: sino-nasal aspergillosis (an infection caused by a fungus) and lymphoplasmacytic rhinitis (a type of inflammation with unclear causes). Researchers compared the nasal tissue of affected dogs to healthy ones to see how gene expression differed. They found that certain genes were more active in dogs with these conditions, which could help explain how the diseases develop. This research may lead to better treatments in the future, but specific treatment options were not detailed in the study.
People also search for: dog nasal discharge treatment · sino-nasal aspergillosis in dogs · lymphoplasmacytic rhinitis in dogs
Abstract
Sino-nasal aspergillosis (SNA) and lymphoplasmacytic rhinitis (LPR) are two common causes of nasal discharge in dog. SNA is typically due to an invasion of Aspergillus fumigatus in the surface of nasal mucosa. The etiology of LPR is poorly understood and a possible implication of fungi is suspected. The purpose of the present study was to explore the immunopathogenesis of these diseases by comparing gene expression in the nasal mucosa from dogs affected by SNA or LPR with healthy dogs, using a canine-specific microarray and quantitative real-time reverse transcriptase polymerase chain reaction for confirmation of the findings of the microarray study. Total RNA was isolated from biopsies of nasal mucosa and gene expression was analyzed via hybridation to the Affymetrix GeneChip(®) Canine Genome 2.0 Array. Selected Affimetrix probes sets identifiers were downloaded into the Database for Annotation, Visualization and Integrated Discovery. Genes of interest were chosen after their fold change and their possible implication in immunopathogenesis of SNA or LPR. The results presented here were in concordance with previous studies on SNA and LPR and highlighted new molecules potentially involved in the pathogenesis of SNA. The over-expression of interleukin (IL)-16, natural killer cell group 7 and chemokine ligand 10 might be related to a potential protective Th1 immunity counterbalanced by other molecules such as DNA-binding protein Ikaros.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/22221380/