Leukocyte and cytokine variables in asymptomatic Pugs at genetic risk of necrotizing meningoencephalitis.


Journal

Journal of veterinary internal medicine
ISSN: 1939-1676
Titre abrégé: J Vet Intern Med
Pays: United States
ID NLM: 8708660

Informations de publication

Date de publication:
Nov 2021
Historique:
revised: 10 10 2021
received: 25 03 2021
accepted: 13 10 2021
pubmed: 24 10 2021
medline: 24 12 2021
entrez: 23 10 2021
Statut: ppublish

Résumé

Necrotizing meningoencephalitis (NME, aka Pug dog encephalitis) is an inflammatory brain condition associated with advanced disease at initial presentation, rapid progression, and poor response to conventional immunomodulatory therapy. That genetic risk for NME, defined by a common germline DNA haplotype located on chromosome 12, is associated with altered blood cytokine concentrations and leukocyte subsets in asymptomatic Pugs. Forty Pug dogs asymptomatic for NME from a hospital sample. Prospective observational cohort study, including germline genome-wide genotyping, plasma cytokine determination by multiplexed profiling, and leukocyte subset characterization by flow cytometric analysis. Seven (18%) dogs were high risk, 10 (25%) medium risk, and 23 (58%) low risk for NME, giving a risk haplotype frequency of 30%. High and medium risk Pugs had significantly lower proportion of CD4+ T cells (median 22% [range, 7.3%-38%] vs 29% [range, 16%-41%], P = .03) and higher plasma IL-10 concentrations than low-risk Pugs (median 14.11 pg/mL [range, 9.66-344.19 pg/mL] vs 12.21 pg/mL [range, 2.59-18.53 pg/mL], P = .001). No other variables were significantly associated with the NME haplotype-based risk. These data suggest an immunological underpinning to NME and a biologic rationale for future clinical trials that investigate novel diagnostic, preventative, and therapeutic strategies for this disease.

Sections du résumé

BACKGROUND BACKGROUND
Necrotizing meningoencephalitis (NME, aka Pug dog encephalitis) is an inflammatory brain condition associated with advanced disease at initial presentation, rapid progression, and poor response to conventional immunomodulatory therapy.
HYPOTHESIS/OBJECTIVES OBJECTIVE
That genetic risk for NME, defined by a common germline DNA haplotype located on chromosome 12, is associated with altered blood cytokine concentrations and leukocyte subsets in asymptomatic Pugs.
ANIMALS METHODS
Forty Pug dogs asymptomatic for NME from a hospital sample.
METHODS METHODS
Prospective observational cohort study, including germline genome-wide genotyping, plasma cytokine determination by multiplexed profiling, and leukocyte subset characterization by flow cytometric analysis.
RESULTS RESULTS
Seven (18%) dogs were high risk, 10 (25%) medium risk, and 23 (58%) low risk for NME, giving a risk haplotype frequency of 30%. High and medium risk Pugs had significantly lower proportion of CD4+ T cells (median 22% [range, 7.3%-38%] vs 29% [range, 16%-41%], P = .03) and higher plasma IL-10 concentrations than low-risk Pugs (median 14.11 pg/mL [range, 9.66-344.19 pg/mL] vs 12.21 pg/mL [range, 2.59-18.53 pg/mL], P = .001). No other variables were significantly associated with the NME haplotype-based risk.
CONCLUSIONS AND CLINICAL IMPORTANCE CONCLUSIONS
These data suggest an immunological underpinning to NME and a biologic rationale for future clinical trials that investigate novel diagnostic, preventative, and therapeutic strategies for this disease.

Identifiants

pubmed: 34687084
doi: 10.1111/jvim.16293
pmc: PMC8692191
doi:

Substances chimiques

Cytokines 0

Types de publication

Journal Article Observational Study, Veterinary

Langues

eng

Sous-ensembles de citation

IM

Pagination

2846-2852

Informations de copyright

© 2021 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals LLC on behalf of American College of Veterinary Internal Medicine.

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Auteurs

Rebecca Windsor (R)

Ethos Veterinary Health, Woburn, Massachusetts, USA.
Ethos Discovery (501c3), San Diego, California, USA.

Samuel D Stewart (SD)

Ethos Veterinary Health, Woburn, Massachusetts, USA.
Ethos Discovery (501c3), San Diego, California, USA.

Joshua Talboom (J)

Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Arizona, USA.

Candace Lewis (C)

Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Arizona, USA.

Marcus Naymik (M)

Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Arizona, USA.

Ignazio S Piras (IS)

Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Arizona, USA.

Stefan Keller (S)

Department of Pathology, Microbiology, Immunology, University of California, Davis, Davis, California, USA.

Dori L Borjesson (DL)

Department of Pathology, Microbiology, Immunology, University of California, Davis, Davis, California, USA.

Gary Clark (G)

Gary Clark Statistical Consulting LLC, Superior, Colorado, USA.

Chand Khanna (C)

Ethos Veterinary Health, Woburn, Massachusetts, USA.
Ethos Discovery (501c3), San Diego, California, USA.

Matthew Huentelman (M)

Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Arizona, USA.

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Classifications MeSH