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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...

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Autores principales: Mulay, Apoorva, Hood, Derek W., Williams, Debbie, Russell, Catherine, Brown, Steve D. M., Bingle, Lynne, Cheeseman, Michael, Bingle, Colin D.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
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.
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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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