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Loss of the homeostatic protein BPIFA1, leads to exacerbation of otitis media severity in the Junbo mouse model
Otitis Media (OM) is characterized by epithelial abnormalities and defects in innate immunity in the middle ear (ME). Although, BPIFA1, a member of the BPI fold containing family of putative innate defence proteins is abundantly expressed by the ME epithelium and SNPs in Bpifa1 have been associated...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5814562/ https://www.ncbi.nlm.nih.gov/pubmed/29449589 http://dx.doi.org/10.1038/s41598-018-21166-7 |
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author | Mulay, Apoorva Hood, Derek W. Williams, Debbie Russell, Catherine Brown, Steve D. M. Bingle, Lynne Cheeseman, Michael Bingle, Colin D. |
author_facet | Mulay, Apoorva Hood, Derek W. Williams, Debbie Russell, Catherine Brown, Steve D. M. Bingle, Lynne Cheeseman, Michael Bingle, Colin D. |
author_sort | Mulay, Apoorva |
collection | PubMed |
description | Otitis Media (OM) is characterized by epithelial abnormalities and defects in innate immunity in the middle ear (ME). Although, BPIFA1, a member of the BPI fold containing family of putative innate defence proteins is abundantly expressed by the ME epithelium and SNPs in Bpifa1 have been associated with OM susceptibility, its role in the ME is not well characterized. We investigated the role of BPIFA1 in protection of the ME and the development of OM using murine models. Loss of Bpifa1 did not lead to OM development. However, deletion of Bpifa1 in Evi1(Jbo/+) mice, a model of chronic OM, caused significant exacerbation of OM severity, thickening of the ME mucosa and increased collagen deposition, without a significant increase in pro-inflammatory gene expression. Our data suggests that BPIFA1 is involved in maintaining homeostasis within the ME under steady state conditions and its loss in the presence of inflammation, exacerbates epithelial remodelling leading to more severe OM. |
format | Online Article Text |
id | pubmed-5814562 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-58145622018-02-21 Loss of the homeostatic protein BPIFA1, leads to exacerbation of otitis media severity in the Junbo mouse model Mulay, Apoorva Hood, Derek W. Williams, Debbie Russell, Catherine Brown, Steve D. M. Bingle, Lynne Cheeseman, Michael Bingle, Colin D. Sci Rep Article Otitis Media (OM) is characterized by epithelial abnormalities and defects in innate immunity in the middle ear (ME). Although, BPIFA1, a member of the BPI fold containing family of putative innate defence proteins is abundantly expressed by the ME epithelium and SNPs in Bpifa1 have been associated with OM susceptibility, its role in the ME is not well characterized. We investigated the role of BPIFA1 in protection of the ME and the development of OM using murine models. Loss of Bpifa1 did not lead to OM development. However, deletion of Bpifa1 in Evi1(Jbo/+) mice, a model of chronic OM, caused significant exacerbation of OM severity, thickening of the ME mucosa and increased collagen deposition, without a significant increase in pro-inflammatory gene expression. Our data suggests that BPIFA1 is involved in maintaining homeostasis within the ME under steady state conditions and its loss in the presence of inflammation, exacerbates epithelial remodelling leading to more severe OM. Nature Publishing Group UK 2018-02-15 /pmc/articles/PMC5814562/ /pubmed/29449589 http://dx.doi.org/10.1038/s41598-018-21166-7 Text en © The Author(s) 2018 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Mulay, Apoorva Hood, Derek W. Williams, Debbie Russell, Catherine Brown, Steve D. M. Bingle, Lynne Cheeseman, Michael Bingle, Colin D. Loss of the homeostatic protein BPIFA1, leads to exacerbation of otitis media severity in the Junbo mouse model |
title | Loss of the homeostatic protein BPIFA1, leads to exacerbation of otitis media severity in the Junbo mouse model |
title_full | Loss of the homeostatic protein BPIFA1, leads to exacerbation of otitis media severity in the Junbo mouse model |
title_fullStr | Loss of the homeostatic protein BPIFA1, leads to exacerbation of otitis media severity in the Junbo mouse model |
title_full_unstemmed | Loss of the homeostatic protein BPIFA1, leads to exacerbation of otitis media severity in the Junbo mouse model |
title_short | Loss of the homeostatic protein BPIFA1, leads to exacerbation of otitis media severity in the Junbo mouse model |
title_sort | loss of the homeostatic protein bpifa1, leads to exacerbation of otitis media severity in the junbo mouse model |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5814562/ https://www.ncbi.nlm.nih.gov/pubmed/29449589 http://dx.doi.org/10.1038/s41598-018-21166-7 |
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