Tuft cells in the pathogenesis of chronic rhinosinusitis with nasal polyps and asthma

被引:15
|
作者
Sell, Elizabeth A. [1 ]
Ortiz-Carpena, Jorge F. [2 ]
Herbert, De'Broski R. [2 ]
Cohen, Noam A. [1 ,3 ,4 ,5 ]
机构
[1] Univ Penn, Perelman Sch Med, 3400 Civ Ctr Blvd, Philadelphia, PA 19104 USA
[2] Univ Penn, Sch Vet Med, Dept Pathobiol, Philadelphia, PA 19104 USA
[3] Univ Penn, Perelman Sch Med, Dept Otorhinolaryngol Head & Neck Surg, Div Rhinol, Philadelphia, PA 19104 USA
[4] US Dept Vet Affairs, Vet Hlth Adm, Corporal Michael J Crescenz Vet Adm Med Ctr, Philadelphia, PA USA
[5] Monell Chem Senses Ctr, 3500 Market St, Philadelphia, PA 19104 USA
基金
美国国家卫生研究院;
关键词
EXACERBATED RESPIRATORY-DISEASE; BITTER TASTE RECEPTORS; CHEMOSENSORY CELLS; IMMUNE-RESPONSES; TYPE-2; IMMUNITY; BRUSH CELLS; SWEET TASTE; EXPRESSION; INTERLEUKIN-25; DOUBLECORTIN;
D O I
10.1016/j.anai.2020.10.011
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Objective: To review the latest discoveries regarding the role of tuft cells in the pathogenesis of chronic rhinosinusitis (CRS) with nasal polyposis and asthma. Data Sources: Reviews and primary research manuscripts were identified from PubMed, Google, and bioRxiv using the search words airway epithelium, nasal polyposis, CRS or asthma and chemoreceptor cell, solitary chemosensory cell, brush cell, microvillus cell, and tuft cell. Study Selections: Studies were selected on the basis of novelty and likely relevance to the functions of tuft cells in chronic inflammatory diseases in the upper and lower airways. Results: Tuft cells coordinate a variety of immune responses throughout the body. After the activation of bitter-taste receptors, tuft cells coordinate the secretion of antimicrobial products by adjacent epithelial cells and initiate the calcium-dependent release of acetylcholine resulting in neurogenic inflammation, including mast cell degranulation and plasma extravasation. Tuft cells are also the dominant source of interleukin-25 and a significant source of cysteinyl leukotrienes that play a role in initiating inflammatory processes in the airway. Tuft cells have also been found to seem de novo in the distal airway after a viral infection, implicating these cells in dysplastic remodeling in the distal lung in the pathogenesis of asthma. Conclusion: Tuft cells bridge innate and adaptive immunes responses and play an upstream role in initiating type 2 inflammation in the upper and possibly the lower airway. The role of tuft cells in respiratory pathophysiology must be further investigated, because tuft cells are putative high-value therapeutic targets for novel therapeutics in CRS with nasal polyps and asthma. (C) 2020 Published by Elsevier Inc. on behalf of American College of Allergy, Asthma & Immunology.
引用
收藏
页码:143 / 151
页数:9
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