{"title":"The advance on pathophysiological mechanisms of type 2 chronic rhinosinusitis with nasal polyposis.","authors":"Cheng Yang, Ling Guo, Yuhan Wang, Wenjing Jiang, Sijia Chen, Qingjia Gu","doi":"10.3389/falgy.2025.1599797","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>This review aims to explore the pathophysiological mechanisms and emerging therapies for type 2 chronic rhinosinusitis with nasal polyps (CRSwNP), driven primarily by type 2 inflammation.</p><p><strong>Search methods: </strong>A comprehensive search of relevant literature was performed in databases including PubMed, Web of Science, and Scopus, using keywords such as \"chronic rhinosinusitis with nasal polyps,\" \"type 2 inflammation,\" \"Th2 cells,\" \"ILC2s,\" \"epithelial barrier dysfunction,\" and \"biologics\". The search was limited to articles published from January 2010 to February 2025.</p><p><strong>Search results: </strong>A total of 200 articles were initially retrieved. After screening based on relevance and quality, 163 articles were selected for this review. These included 109 basic research papers, 30 clinical studies, and 24 review articles.</p><p><strong>Conclusions: </strong>Type 2 CRSwNP pathogenesis involves Th2/ILC2-IL-4/IL-13 synergy, driving eosinophilic inflammation and tissue remodeling via a self-amplifying loop. Programmed cell death protein 1 and programmed death-ligand 1 dysregulation intensifies Th2 responses. Epithelial barrier defects (via disrupted junctions and ciliary defects) and epithelial-mesenchymal transition facilitate pathogen invasion and stromal changes. M2 macrophages amplify inflammation via CCL-24 and <i>Staphylococcus aureus</i> synergy, sustaining biofilm persistence. Targeted biologics-dupilumab (IL-4Rα inhibitor) reduces polyp burden and restores smell, while mepolizumab (anti-IL-5) and omalizumab (anti-IgE) address specific endotypes. Despite therapeutic advances, biologics require real-world validation for long-term safety and cost-effectiveness.</p>","PeriodicalId":73062,"journal":{"name":"Frontiers in allergy","volume":"6 ","pages":"1599797"},"PeriodicalIF":3.3000,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12263562/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in allergy","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3389/falgy.2025.1599797","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"ALLERGY","Score":null,"Total":0}
引用次数: 0
Abstract
Purpose: This review aims to explore the pathophysiological mechanisms and emerging therapies for type 2 chronic rhinosinusitis with nasal polyps (CRSwNP), driven primarily by type 2 inflammation.
Search methods: A comprehensive search of relevant literature was performed in databases including PubMed, Web of Science, and Scopus, using keywords such as "chronic rhinosinusitis with nasal polyps," "type 2 inflammation," "Th2 cells," "ILC2s," "epithelial barrier dysfunction," and "biologics". The search was limited to articles published from January 2010 to February 2025.
Search results: A total of 200 articles were initially retrieved. After screening based on relevance and quality, 163 articles were selected for this review. These included 109 basic research papers, 30 clinical studies, and 24 review articles.
Conclusions: Type 2 CRSwNP pathogenesis involves Th2/ILC2-IL-4/IL-13 synergy, driving eosinophilic inflammation and tissue remodeling via a self-amplifying loop. Programmed cell death protein 1 and programmed death-ligand 1 dysregulation intensifies Th2 responses. Epithelial barrier defects (via disrupted junctions and ciliary defects) and epithelial-mesenchymal transition facilitate pathogen invasion and stromal changes. M2 macrophages amplify inflammation via CCL-24 and Staphylococcus aureus synergy, sustaining biofilm persistence. Targeted biologics-dupilumab (IL-4Rα inhibitor) reduces polyp burden and restores smell, while mepolizumab (anti-IL-5) and omalizumab (anti-IgE) address specific endotypes. Despite therapeutic advances, biologics require real-world validation for long-term safety and cost-effectiveness.
目的：本综述旨在探讨主要由2型炎症驱动的2型慢性鼻窦炎伴鼻息肉（CRSwNP）的病理生理机制和新兴治疗方法。检索方法：在PubMed、Web of Science、Scopus等数据库中全面检索相关文献，检索关键词为“慢性鼻窦炎合并鼻息肉”、“2型炎症”、“Th2细胞”、“ILC2s”、“上皮屏障功能障碍”、“生物制剂”等。检索仅限于2010年1月至2025年2月期间发表的文章。搜索结果：最初总共检索到200篇文章。根据相关性和质量筛选后，163篇文章入选本综述。其中包括109篇基础研究论文、30篇临床研究论文和24篇综述文章。结论：2型CRSwNP发病机制涉及Th2/ILC2-IL-4/IL-13协同作用，通过自我放大回路驱动嗜酸性粒细胞炎症和组织重塑。程序性细胞死亡蛋白1和程序性死亡配体1失调加剧了Th2反应。上皮屏障缺陷（通过破坏连接和纤毛缺陷）和上皮-间质转化促进病原体侵袭和间质改变。M2巨噬细胞通过CCL-24和金黄色葡萄球菌的协同作用放大炎症，维持生物膜的持久性。靶向生物制剂-dupilumab （IL-4Rα抑制剂）可减轻息肉负担并恢复嗅觉，而mepolizumab（抗il -5）和omalizumab（抗ige）可解决特定的内源性疾病。尽管在治疗方面取得了进步，但生物制剂需要在现实世界中进行长期安全性和成本效益的验证。
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