Immunopathogenesis of canine chronic ulcerative stomatitis.

Canine Chronic Ulcerative Stomatitis is a spontaneously occurring inflammatory disease of the oral mucosa. An immune-mediated pathogenesis is suspected though not yet proven. We have recently reported on the clinical and histologic features, and identification of select leukocyte cell populations wi...

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Main Authors: J G Anderson, A Kol, P Bizikova, B P Stapelton, K Ford, A Villarreal, R J Jimenez, D Vasilatis, B G Murphy
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2020-01-01
Series:PLoS ONE
Online Access:https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0227386&type=printable
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author J G Anderson
A Kol
P Bizikova
B P Stapelton
K Ford
A Villarreal
R J Jimenez
D Vasilatis
B G Murphy
author_facet J G Anderson
A Kol
P Bizikova
B P Stapelton
K Ford
A Villarreal
R J Jimenez
D Vasilatis
B G Murphy
author_sort J G Anderson
collection DOAJ
description Canine Chronic Ulcerative Stomatitis is a spontaneously occurring inflammatory disease of the oral mucosa. An immune-mediated pathogenesis is suspected though not yet proven. We have recently reported on the clinical and histologic features, and identification of select leukocyte cell populations within the lesion. A clinical and histologic similarity to oral lichen planus of people was proposed. In the present study, these initial observations are extended by examining lesions from 24 dogs with clinical evidence of chronic ulcerative stomatitis. Because dogs with chronic ulcerative stomatitis often have concurrent periodontal disease, we wondered if dental plaque/biofilm may be a common instigator of inflammation in both lesions. We hypothesized that dogs with chronic ulcerative stomatitis would exhibit a spectrum of pathologic changes and phenotype of infiltrating leukocytes that would inform lesion pathogenesis and that these changes would differ from inflammatory phenotypes in periodontitis. Previously we identified chronic ulcerative stomatitis lesions to be rich in FoxP3+ and IL17+ cells. As such, we suspect that these leukocytes play an important role in lesion pathogenesis. The current study confirms the presence of moderate to large numbers of FoxP3+ T cells and IL17+ cells in all ulcerative stomatitis lesions using confocal immunofluorescence. Interestingly, the majority of IL17+ cells were determined to be non-T cells and IL17+ cell frequencies were negatively correlated with severity on the clinical scoring system. Three histologic subtypes of ulcerative stomatitis were determined; lichenoid, deep stomatitis and granulomatous. Periodontitis lesions, like stomatitis lesions, were B cell and plasma cell rich, but otherwise differed from the stomatitis lesions. Direct immunofluorescence results did not support an autoantibody-mediated autoimmune disease process. This investigation contributes to the body of literature regarding leukocyte involvement in canine idiopathic inflammatory disease pathogenesis.
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spelling doaj-art-cd1b58f7cf7044bf87a0066e296b83892025-08-20T02:11:20ZengPublic Library of Science (PLoS)PLoS ONE1932-62032020-01-01151e022738610.1371/journal.pone.0227386Immunopathogenesis of canine chronic ulcerative stomatitis.J G AndersonA KolP BizikovaB P StapeltonK FordA VillarrealR J JimenezD VasilatisB G MurphyCanine Chronic Ulcerative Stomatitis is a spontaneously occurring inflammatory disease of the oral mucosa. An immune-mediated pathogenesis is suspected though not yet proven. We have recently reported on the clinical and histologic features, and identification of select leukocyte cell populations within the lesion. A clinical and histologic similarity to oral lichen planus of people was proposed. In the present study, these initial observations are extended by examining lesions from 24 dogs with clinical evidence of chronic ulcerative stomatitis. Because dogs with chronic ulcerative stomatitis often have concurrent periodontal disease, we wondered if dental plaque/biofilm may be a common instigator of inflammation in both lesions. We hypothesized that dogs with chronic ulcerative stomatitis would exhibit a spectrum of pathologic changes and phenotype of infiltrating leukocytes that would inform lesion pathogenesis and that these changes would differ from inflammatory phenotypes in periodontitis. Previously we identified chronic ulcerative stomatitis lesions to be rich in FoxP3+ and IL17+ cells. As such, we suspect that these leukocytes play an important role in lesion pathogenesis. The current study confirms the presence of moderate to large numbers of FoxP3+ T cells and IL17+ cells in all ulcerative stomatitis lesions using confocal immunofluorescence. Interestingly, the majority of IL17+ cells were determined to be non-T cells and IL17+ cell frequencies were negatively correlated with severity on the clinical scoring system. Three histologic subtypes of ulcerative stomatitis were determined; lichenoid, deep stomatitis and granulomatous. Periodontitis lesions, like stomatitis lesions, were B cell and plasma cell rich, but otherwise differed from the stomatitis lesions. Direct immunofluorescence results did not support an autoantibody-mediated autoimmune disease process. This investigation contributes to the body of literature regarding leukocyte involvement in canine idiopathic inflammatory disease pathogenesis.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0227386&type=printable
spellingShingle J G Anderson
A Kol
P Bizikova
B P Stapelton
K Ford
A Villarreal
R J Jimenez
D Vasilatis
B G Murphy
Immunopathogenesis of canine chronic ulcerative stomatitis.
PLoS ONE
title Immunopathogenesis of canine chronic ulcerative stomatitis.
title_full Immunopathogenesis of canine chronic ulcerative stomatitis.
title_fullStr Immunopathogenesis of canine chronic ulcerative stomatitis.
title_full_unstemmed Immunopathogenesis of canine chronic ulcerative stomatitis.
title_short Immunopathogenesis of canine chronic ulcerative stomatitis.
title_sort immunopathogenesis of canine chronic ulcerative stomatitis
url https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0227386&type=printable
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