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Transcriptomic signatures of feline chronic gingivostomatitis are influenced by upregulated IL6
Feline chronic gingivostomatitis (FCGS) is a relatively common and debilitating disease characterized by bilateral inflammation and ulceration of the caudal oral mucosa, alveolar and buccal mucosa, and varying degrees of periodontal disease. The etiopathogenesis of FCGS remains unresolved. In this s...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10439118/ https://www.ncbi.nlm.nih.gov/pubmed/37596310 http://dx.doi.org/10.1038/s41598-023-40679-4 |
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author | Peralta, Santiago Grenier, Jennifer K. Webb, Suzin M. Miller, Andrew D. Miranda, Ileana C. Parker, John S. L. |
author_facet | Peralta, Santiago Grenier, Jennifer K. Webb, Suzin M. Miller, Andrew D. Miranda, Ileana C. Parker, John S. L. |
author_sort | Peralta, Santiago |
collection | PubMed |
description | Feline chronic gingivostomatitis (FCGS) is a relatively common and debilitating disease characterized by bilateral inflammation and ulceration of the caudal oral mucosa, alveolar and buccal mucosa, and varying degrees of periodontal disease. The etiopathogenesis of FCGS remains unresolved. In this study, we performed bulk RNA-seq molecular profiling of affected tissues derived from a cohort of client-owned cats with FCGS compared to tissues from unaffected animals, to identify candidate genes and pathways that can help guide future exploration of novel clinical solutions. We complemented transcriptomic findings with immunohistochemistry and in situ hybridization assays to better understand the biological significance of the results and performed RNA-seq validation of biologically relevant differentially expressed genes using qPCR assays to demonstrate technical reproducibility. Transcriptomic profiles of oral mucosal tissues in cats with FCGS are enriched with immune- and inflammation-related genes and pathways that appear to be largely influenced by IL6, and include NFKB, JAK/STAT, IL-17 and IFN type I and II signaling, offering new opportunities to develop novel clinical applications based on a more rational understanding of the disease. |
format | Online Article Text |
id | pubmed-10439118 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-104391182023-08-20 Transcriptomic signatures of feline chronic gingivostomatitis are influenced by upregulated IL6 Peralta, Santiago Grenier, Jennifer K. Webb, Suzin M. Miller, Andrew D. Miranda, Ileana C. Parker, John S. L. Sci Rep Article Feline chronic gingivostomatitis (FCGS) is a relatively common and debilitating disease characterized by bilateral inflammation and ulceration of the caudal oral mucosa, alveolar and buccal mucosa, and varying degrees of periodontal disease. The etiopathogenesis of FCGS remains unresolved. In this study, we performed bulk RNA-seq molecular profiling of affected tissues derived from a cohort of client-owned cats with FCGS compared to tissues from unaffected animals, to identify candidate genes and pathways that can help guide future exploration of novel clinical solutions. We complemented transcriptomic findings with immunohistochemistry and in situ hybridization assays to better understand the biological significance of the results and performed RNA-seq validation of biologically relevant differentially expressed genes using qPCR assays to demonstrate technical reproducibility. Transcriptomic profiles of oral mucosal tissues in cats with FCGS are enriched with immune- and inflammation-related genes and pathways that appear to be largely influenced by IL6, and include NFKB, JAK/STAT, IL-17 and IFN type I and II signaling, offering new opportunities to develop novel clinical applications based on a more rational understanding of the disease. Nature Publishing Group UK 2023-08-18 /pmc/articles/PMC10439118/ /pubmed/37596310 http://dx.doi.org/10.1038/s41598-023-40679-4 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Peralta, Santiago Grenier, Jennifer K. Webb, Suzin M. Miller, Andrew D. Miranda, Ileana C. Parker, John S. L. Transcriptomic signatures of feline chronic gingivostomatitis are influenced by upregulated IL6 |
title | Transcriptomic signatures of feline chronic gingivostomatitis are influenced by upregulated IL6 |
title_full | Transcriptomic signatures of feline chronic gingivostomatitis are influenced by upregulated IL6 |
title_fullStr | Transcriptomic signatures of feline chronic gingivostomatitis are influenced by upregulated IL6 |
title_full_unstemmed | Transcriptomic signatures of feline chronic gingivostomatitis are influenced by upregulated IL6 |
title_short | Transcriptomic signatures of feline chronic gingivostomatitis are influenced by upregulated IL6 |
title_sort | transcriptomic signatures of feline chronic gingivostomatitis are influenced by upregulated il6 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10439118/ https://www.ncbi.nlm.nih.gov/pubmed/37596310 http://dx.doi.org/10.1038/s41598-023-40679-4 |
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