Increased Expression of Toll-Like Receptors 2 and 4 and Related Cytokines in Persistent Allergic Rhinitis. (February 2015)

• Record Type: Journal Article
• Authors: Cui, Xin-Yan; Chen, Xi; Yu, Chen-Jie; Yang, Jun; Lin, Zi-Ping; Yin, Min; Cheng, Lei
• Is Part Of: Otolaryngology--head and neck surgery. Volume 152:Number 2(2015:Feb.)
• Page Start: 233
• Page End: 238
• Publication Date: 2015-02
• Subjects: Toll-like receptors -- persistent allergic rhinitis -- innate immunity -- cytokines -- nasal mucosa; Head -- Surgery -- Periodicals; Neck -- Surgery -- Periodicals; Otolaryngology -- Periodicals; 617.51
• DOI: 10.1177/0194599814562173
• Languages: English
• ISSNs: 0194-5998

Abstract

Objectives: 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). Study Design: Experimental study of human nasal tissue. Setting: Academic medical center. Subjects and Methods: 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. Results: 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. Conclusion: 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.