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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 <jats:italic>Bpifa1<\/jats:italic> 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 <jats:italic>Bpifa1<\/jats:italic> did not lead to OM development. However, deletion of <jats:italic>Bpifa1<\/jats:italic> in <jats:italic>Evi1<\/jats:italic><jats:sup>Jbo\/+<\/jats:sup> 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.<\/jats:p>","DOI":"10.1038\/s41598-018-21166-7","type":"journal-article","created":{"date-parts":[[2018,2,9]],"date-time":"2018-02-09T16:29:15Z","timestamp":1518193755000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Loss of the homeostatic protein BPIFA1, leads to exacerbation of otitis media severity in the Junbo mouse model"],"prefix":"10.1038","volume":"8","author":[{"given":"Apoorva","family":"Mulay","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Derek W.","family":"Hood","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Debbie","family":"Williams","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Catherine","family":"Russell","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steve D. 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