Increased Expression of Toll‐Like Receptors 2 and 4 and Related Cytokines in Persistent Allergic Rhinitis

TLR2型 TLR4型 信使核糖核酸 受体 鼻粘膜 免疫组织化学 Toll样受体 促炎细胞因子 肿瘤坏死因子α 细胞因子 逆转录聚合酶链式反应 免疫学 免疫系统 白细胞介素 医学 炎症 先天免疫系统 生物 内科学 基因 生物化学
作者
Xinyan Cui,Xi Chen,Chenjie Yu,Jun Yang,Ziping Lin,Min Yin,Lei Cheng
出处
期刊:Otolaryngology-Head and Neck Surgery [Wiley]
卷期号:152 (2): 233-238 被引量:25
标识
DOI:10.1177/0194599814562173
摘要

Toll-like receptors (TLRs) are the crucial components of host defenses and supposed to play a role in nasal inflammation such as chronic rhinosinusitis and seasonal allergic rhinitis. This study was performed to investigate the expression patterns of TLRs and related cytokines in persistent allergic rhinitis (PER).Experimental study of human nasal tissue.Academic medical center.Nasal biopsy specimens were obtained from 21 patients with PER and 21 controls from December 2012 to September 2013. Messenger RNA (mRNA) expression of TLR1-9, interleukin (IL)-1, IL-6, IL-8, IL-12, interferon (IFN)-α, and tumor necrosis factor (TNF)-α was determined by quantitative reverse transcription polymerase chain reaction. The cellular localizations as well as protein expression of TLR2 and TLR4 were further detected by immunohistochemistry and Western blotting, respectively.TLR1-9 mRNA could be determined in nasal mucosa. Compared with the controls, mRNA expression of only TLR2 and TLR4 was significant higher in patients with PER (P < .05). In addition, mRNA expression of IL-6 and IL-8, but not IL-1, IL-12, IFN-α, and TNF-α, was upregulated in patients with PER vs control subjects (P < .05). However, these increased cytokines were not correlated with either TLR2 or TLR4 in patients with PER. Protein expression of TLR2 and TLR4 was consistent with mRNA levels (P < .05). The cellular distributions of TLR2 and TLR4 were localized in nasal epithelium, subepithelial glands and capillary endothelial cells, and immune cells.TLR2 and TLR4 are increased in patients with PER and may be one of the major contributors to the persistence and aggravation of allergic inflammation in PER.
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