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咽上磨蚀疗法下调 Cav1.2 的表达:流感病毒进入的关键分子。

Epipharyngeal Abrasive Therapy Down-regulates the Expression of Cav1.2: A Key Molecule in Influenza Virus Entry.

机构信息

Section of Otolaryngology, Department of Medicine, Fukuoka Dental College, Fukuoka, Japan;

Nishi Otolaryngology Clinic, Fukuoka, Japan.

出版信息

In Vivo. 2022 Sep-Oct;36(5):2357-2364. doi: 10.21873/invivo.12967.

Abstract

BACKGROUND/AIM: Influenza A virus (IAV) infection causes an inflammatory response to the respiratory mucosa. The viral glycoprotein hemagglutinin (HA) binds to the sialylated voltage-dependent Ca channel (Cav1.2) in ciliated epithelium. The binding of HA and sialylated Cav1.2 is considered essential to IAV infection, entry, and IAV-induced Ca oscillation. The epipharynx comprises the ciliated epithelium, which is the initial target for viruses that cause upper respiratory tract infections. Previously, we showed that epipharyngeal abrasive therapy (EAT), a treatment for chronic epipharyngitis in Japan, which scratches the epipharyngeal mucosa with a cotton swab containing zinc chloride, induces squamous metaplasia. In this study, we evaluated whether squamous metaplasia by EAT affects the expression patterns of Cav1.2.

PATIENTS AND METHODS

The study subjects were seven patients who had not been treated with EAT and 11 patients who had. For the immunohistochemical assessment of the epipharyngeal mucosa, the staining intensity of Cav1.2 was described using the immunohistochemical score (IHC score).

RESULTS

The IHC scores for Cav1.2 in the EAT-treated group was 4.19-fold lower than those in the non-treated group (p=0.0034).

CONCLUSION

EAT down-regulates the expression of Cav1.2, a key cell surface molecule in influenza virus entry via squamous metaplasia. Thus, EAT may be a simple method for preventing influenza infection.

摘要

背景/目的:甲型流感病毒(IAV)感染会引起呼吸道黏膜的炎症反应。病毒糖蛋白血凝素(HA)与纤毛上皮中的唾液酸化电压依赖性钙通道(Cav1.2)结合。HA 与唾液酸化 Cav1.2 的结合被认为是 IAV 感染、进入和 IAV 诱导的 Ca 振荡所必需的。咽上部包括纤毛上皮,这是引起上呼吸道感染的病毒的初始靶标。先前,我们表明,咽上部摩擦疗法(EAT),一种治疗日本慢性咽上部炎的方法,用含有氯化锌的棉签刮擦咽上部黏膜,可诱导鳞状上皮化生。在这项研究中,我们评估了 EAT 引起的鳞状上皮化生是否会影响 Cav1.2 的表达模式。

患者和方法

研究对象为 7 名未接受 EAT 治疗的患者和 11 名接受 EAT 治疗的患者。为了评估咽上部黏膜的免疫组织化学,使用免疫组织化学评分(IHC 评分)描述 Cav1.2 的染色强度。

结果

EAT 治疗组的 Cav1.2 的 IHC 评分比未治疗组低 4.19 倍(p=0.0034)。

结论

EAT 通过鳞状上皮化生下调了流感病毒进入的关键细胞表面分子 Cav1.2 的表达。因此,EAT 可能是预防流感感染的简单方法。

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