Lee Sung Bu, Song Jeong-Ah, Choi Go-Eun, Kim Hun Sik, Jang Yong Ju
Department of Otolaryngology, Yuseoung Sun General Hospital, Daejeon, Republic of Korea.
Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Int Forum Allergy Rhinol. 2016 Nov;6(11):1131-1138. doi: 10.1002/alr.21805. Epub 2016 Jun 27.
Patients with chronic rhinosinusitis (CRS) commonly experience aggravation of their symptoms after viral upper respiratory infection (URI). Rhinovirus (RV) is the most common URI-causing virus. However, there is a lack of a mouse model of RV infection and in vivo studies investigating the effect of RV infection on CRS.
A mouse model of chronic allergic rhinosinusitis (CARS) was established by sensitizing to ovalbumin (OVA) through intraperitoneal injection followed by nasal challenges with OVA for 5 weeks. Both control and CARS mice were euthanized at 48 hours after infection with minor group RV serotype 1B (RV1B). Sinonasal complex samples were evaluated histologically; and interleukin (IL)-6, macrophage inflammatory protein (MIP)-2, IL-13, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ were measured in the nasal lavage fluid. The RV1B-infected areas in control and CARS mice were identified using immunofluorescence.
In the infected control mice group, RV1B increased secretory hyperplasia in the sinonasal mucosa and the production of proinflammatory cytokines including INF-γ, MIP-2, and IL-13. Immunohistochemical analysis of nasal mucosa from RV1B-infected mice presented abundant RV1B staining, which was distributed between the epithelium and the lamina propria. In the CARS group, the RV1B-infected area per unit was significantly higher than that in control mice. However, RV1B infection neither increased the proinflammatory cytokine secretion nor worsened the histology significantly.
We successfully established a mouse model of upper airway RV infection by nasal inoculation with RV1B. Although there was histologically-proven increased RV infection in the CARS model, the infection did not intensify sinonasal inflammation.
慢性鼻-鼻窦炎（CRS）患者在上呼吸道病毒感染（URI）后通常会出现症状加重。鼻病毒（RV）是引起URI最常见的病毒。然而，目前缺乏RV感染的小鼠模型以及研究RV感染对CRS影响的体内研究。
通过腹腔注射卵清蛋白（OVA）致敏，随后用OVA进行鼻腔激发5周，建立慢性变应性鼻-鼻窦炎（CARS）小鼠模型。对照组和CARS小鼠在感染小群RV血清型1B（RV1B）后48小时处死。对鼻窦复合体样本进行组织学评估；并检测鼻灌洗液中的白细胞介素（IL）-6、巨噬细胞炎性蛋白（MIP）-2、IL-13、肿瘤坏死因子（TNF）-α和干扰素（IFN）-γ。采用免疫荧光法鉴定对照组和CARS小鼠中RV1B感染区域。
在感染的对照组小鼠中，RV1B增加了鼻窦黏膜的分泌性增生以及包括INF-γ、MIP-2和IL-13在内的促炎细胞因子的产生。对RV1B感染小鼠鼻黏膜的免疫组织化学分析显示有丰富的RV1B染色，分布于上皮和固有层之间。在CARS组中，单位面积的RV1B感染区域显著高于对照小鼠。然而，RV1B感染既未增加促炎细胞因子的分泌，也未使组织学改变明显加重。
我们通过鼻内接种RV1B成功建立了上呼吸道RV感染的小鼠模型。尽管在CARS模型中有组织学证据表明RV感染增加，但该感染并未加剧鼻窦炎症。
