Loss of the homeostatic protein BPIFA1, leads to exacerbation of otitis media severity in the Junbo mouse model.

Loss of the homeostatic protein BPIFA1, leads to exacerbation of otitis media severity in the Junbo mouse model.
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DOI:
10.1038/s41598-018-21166-7
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发表时间:
2018-02-15
期刊:
影响因子:
4.6
通讯作者:
Bingle CD
Bingle CD
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Mulay A;Hood DW;Williams D;Russell C;Brown SDM;Bingle L;Cheeseman M;Bingle CD

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中耳炎(OM)的特征在于中耳(ME)中的上皮异常和先天免疫缺陷。虽然,BPIFA 1,一个成员的BPI折叠包含家庭的推定先天防御蛋白是丰富的ME上皮细胞和SNPs在Bpifa 1已与OM易感性,它的作用在ME没有得到很好的表征。我们使用小鼠模型研究了BPIFA 1在ME保护和OM发展中的作用。Bpifa 1的缺失不会导致OM的发生。然而,在Evi 1 Jbo/+小鼠(一种慢性OM模型)中,Bpifa 1的缺失导致OM严重程度显著加重、ME粘膜增厚和胶原沉积增加,而促炎基因表达没有显著增加。我们的数据表明,BPIFA 1参与在稳态条件下维持ME内的稳态,并且在炎症存在下其损失加剧上皮重塑,导致更严重的OM。
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 Evi1Jbo/+ 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.
DOI: 10.1242/dmm.026658
发表时间: 2016-11-01
影响因子: 4.3
作者:
Mulay A;Akram KM;Williams D;Armes H;Russell C;Hood D;Armstrong S;Stewart JP;Brown SD;Bingle L;Bingle CD
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影响因子: 3.6
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发表时间: 2005-03-01
影响因子: 7.3
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