Siti Sarah Che Othman, Md Shukri Norasnieda, Mohd Ashari Noor Suryani, Wong Kah Keng
Department of Immunology, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia.
Department of Otorhinolaryngology, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia.
PeerJ. 2020 Sep 4;8:e9834. doi: 10.7717/peerj.9834. eCollection 2020.
Allergic rhinitis (AR) is a common disease affecting 400 million of the population worldwide. Nasal epithelial cells form a barrier against the invasion of environmental pathogens. These nasal epithelial cells are connected together by tight junction (TJ) proteins including zonula occludens-1 (ZO-1), ZO-2 and ZO-3. Impairment of ZO proteins are observed in AR patients whereby dysfunction of ZOs allows allergens to pass the nasal passage into the subepithelium causing AR development. In this review, we discuss ZO proteins and their impairment leading to AR, regulation of their expression by Th1 cytokines (i.e., IL-2, TNF- and IFN-), Th2 cytokines (i.e., IL-4 and IL-13) and histone deacetylases (i.e., HDAC1 and HDAC2). These findings are pivotal for future development of targeted therapies by restoring ZO protein expression and improving nasal epithelial barrier integrity in AR patients.
变应性鼻炎（AR）是一种常见疾病，全球有4亿人受其影响。鼻上皮细胞形成一道抵御环境病原体入侵的屏障。这些鼻上皮细胞通过紧密连接（TJ）蛋白连接在一起，包括闭合蛋白-1（ZO-1）、ZO-2和ZO-3。在AR患者中观察到ZO蛋白受损，ZO功能障碍使过敏原通过鼻腔进入上皮下，导致AR发生。在本综述中，我们讨论了ZO蛋白及其受损导致AR的情况，Th1细胞因子（即白细胞介素-2、肿瘤坏死因子和干扰素-）、Th2细胞因子（即白细胞介素-4和白细胞介素-13）和组蛋白脱乙酰酶（即HDAC1和HDAC2）对其表达的调节。这些发现对于未来通过恢复ZO蛋白表达和改善AR患者鼻上皮屏障完整性来开发靶向治疗至关重要。
