Viral disruption of olfactory progenitors is exacerbated in allergic mice.

Viral disruption of olfactory progenitors is exacerbated in allergic mice.
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在过敏小鼠中,病毒对嗅觉祖细胞的破坏更加严重。

DOI:
10.1016/j.intimp.2014.06.034
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发表时间:
2014
影响因子:
5.6
通讯作者:
Kunkel,SL
Kunkel,SL
中科院分区:
医学2区
文献类型:
--
作者:
Ueha,R;Mukherjee,S;Ueha,S;deAlmeidaNagata,DE;Sakamoto,T;Kondo,K;Yamasoba,T;Lukacs,NW;Kunkel,SL

文献摘要

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呼吸道过敏患者的上呼吸道病毒感染通常会加重嗅觉功能障碍,但这种加重的机制尚不清楚。在这里,我们研究了呼吸道合胞病毒(RSV)感染,在存在或不存在呼吸道过敏的情况下,对小鼠嗅觉感受器神经元(ON)及其祖细胞的影响。免疫组织化学分析显示,蟑螂变应原(CRA)单独诱导的气道变态反应不影响OMP+成熟Orn和SOX2+ORN祖细胞的数量。无过敏小鼠鼻内感染RSV 19株可导致SOX2+ORN祖细胞一过性减少,但不影响OMP+ORN细胞。相反,RSV诱导的SOX2+ORN祖细胞的减少在过敏小鼠中加剧和延长,最终导致OMP+ORN的丢失。在过敏小鼠中,与非过敏小鼠相比,嗅觉上皮细胞中RSV的减少延迟。这些结果表明,呼吸道合胞病毒感染会损害ORN祖细胞,而呼吸道变态反应通过减少病毒清除而加重对ORN祖细胞的损害。
Upper airway viral infection in patients with airway allergy often exacerbates olfactory dysfunction, but the mechanism for this exacerbation remains unclear. Here, we examined the effects of respiratory syncytial virus (RSV) infection, in the presence or absence of airway allergy, on olfactory receptor neurons (ORNs) and their progenitors in mice. Immunohistological analyses revealed that cockroach allergen (CRA)-induced airway allergy alone did not affect the number of OMP+mature ORNs and SOX2+ORN progenitors. Intranasal RSV line 19 infection in allergy-free mice resulted in a transient decrease in SOX2+ORN progenitors without affecting OMP+ORNs. In contrast, the RSV-induced decrease in SOX2+ORN progenitors was exacerbated and prolonged in allergic mice, which resulted in eventual loss of OMP+ORNs. In the allergic mice, reduction of RSV in the olfactory epithelium was delayed as compared with allergy-free mice. These results suggest that ORN progenitors were impaired by RSV infection and that airway allergy exacerbated damage to ORN progenitors by reducing viral clearance.