Genetics of denatonium-responsive bitter receptors in aspirin-exacerbated respiratory disease.
Genetics of denatonium-responsive bitter receptors in aspirin-exacerbated respiratory disease.
复制标题
阿司匹林加剧的呼吸道疾病中地那铵反应性苦味受体的遗传学。
DOI：
10.1002/alr.23077
复制
发表时间：
2023
影响因子：
6.4
通讯作者：
Cohen,NoamA
中科院分区：
文献类型：
--
作者：
Douglas,JenniferE;Lin,Cailu;Mansfield,CorrineJ;Bell,Katherine;Salmon,MandyK;Kohanski,MichaelA;Adappa,NithinD;Palmer,JamesN;Bosso,JohnV;Reed,DanielleR;Cohen,NoamA
Chronic rhinosinusitis (CRS), a disease of long-standing sinonasal inflammation, is divided into two phenotypes: CRS with and without nasal polyposis (CRSwNP, CRSsNP). A unique sub-type of CRSwNP consists of a treatment-recalcitrant form termed aspirin-exacerbated respiratory disease (AERD), typified by polyposis, asthma, and sensitivity to non-steroidal anti-inflammatory drugs. 1The upper airway attempts to combat invading pathogens through mucociliary clearance (MCC) and the secretion of bactericidal compounds (nitric oxide (NO), anti-microbial peptides (AMPs)). 2 Prior studies show that genetic variation in bitter taste receptors (T2Rs) contributes to the vigor of sinonasal immune response. The solitary chemosensory cell (SCC) is a heavily innervated, pro-inflammatory cell in the sinonasal epithelium which expresses T2Rs. 3 Activation of SCC-based T2Rs drives AMP secretion and type-2 inflammation through IL-25 secretion and mast cell activation. 4 Recent work has demonstrated that SCCs are the exclusive epithelial source of IL-25 which, together with IL-33 and thymic stromal lipoprotein, stimulate type 2 innate lymphoid cells to secrete IL-13 and drive eosinophilic chemotaxis. 4, 5 Studies additionally show polyps are enriched in SCCs. 4
