Article record

评估慢性鼻窦炎中肥胖的黏膜炎症内型

Assessing the Mucosal Inflammatory Endotype of Obesity in Chronic Rhinosinusitis.

临床研究鼻科IF 4.9Q1

文献信息

PMID	42855728
原文	在 PubMed 查看原文 ↗
发表日期	2026
作者	Jeffanie W Gayoso 查看其他 9 位作者 Li-Ching Huang；Quanhu Sheng；Daniel Lofgren；Ping Li；Katherine Cahill；Mason Krysinski；Rakesh K Chandra；Justin H Turner；Naweed Chowdhury
作者单位	Department of Otolaryngology-Head and Neck Surgery, Vanderbilt University Medical Center, Nashville, Tennessee, USA. 查看其他 4 条单位信息 Department of Biostatistics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.；Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.；Department of Otolaryngology-Head and Neck Surgery, University of Mississippi Medical Center, Jackson, Mississippi, USA.；Department of Otolaryngology-Head and Neck Surgery, University of Alabama at Birmingham, Birmingham, Alabama, USA.
期刊	International forum of allergy & rhinology
SCI 分区	Q1
IF	4.9
研究类型	临床研究 · 临床
所属专科	鼻科

中文摘要

背景： 慢性鼻窦炎（CRS）是一种异质性炎症综合征，累及鼻窦，表型上定义为伴鼻息肉（CRSwNP）或不伴鼻息肉（CRSsNP）。近年来，炎症标志物已被用于将患者聚类为推测具有共同潜在病因的假定内型。已知肥胖在类似的慢性炎症性疾病（如哮喘）中会产生促炎状态。然而，肥胖在CRS中的潜在影响尚未被研究。
方法： 在一项前瞻性纵向研究中，从512例CRS患者（235例CRSsNP，277例CRSwNP）和100例接受手术的对照患者中收集样本。使用靶向IL-1a、IL-1b、IL-2、IL-3、IL-4、IL-5、IL-6、IL-7、IL-8、IL-9、IL-10、IL-11、IL-12、IL-13、IL-17、IL-18、IL-21、TNF-⍺、IFN-𝛾、eotaxin、RANTES和GM-CSF的多重细胞珠测定法测量黏液炎症细胞因子。然后使用BMI的分类和连续测量比较肥胖与非肥胖患者之间的细胞因子水平。
结果： 在CRSwNP患者中，多种促炎细胞因子显著升高。肥胖CRSwNP患者的IL-2（185 pg/mL vs. 39 pg/mL，p = 0.02）、IL-4（17.7 pg/mL vs. 6.3 pg/mL，p = 0.04）、TNF-⍺（58 pg/mL vs. 45 pg/mL，p = 0.04）、IFN-ɣ（18.5 pg/mL vs. 17.3 pg/mL，p = 0.009）和GM-CSF（8.5 pg/mL vs. 2.5 pg/mL，p = 0.007）水平升高。连续回归分析未证实这些结果，可能是由于肥胖对鼻窦炎症的非线性效应。
结论： 与非肥胖患者相比，肥胖CRSwNP患者的1型和2型细胞因子升高，可能提示肥胖患者鼻窦黏膜存在促炎偏倚。因此，减重和医学体重管理可能在CRSwNP的治疗中发挥作用，尽管需要进一步研究。

英文摘要

BACKGROUND: Chronic rhinosinusitis (CRS) is a heterogeneous inflammatory syndrome of the paranasal sinuses that is defined phenotypically as either with nasal polyps (CRSwNP) or without nasal polyps (CRSsNP). More recently, inflammatory markers have been used to cluster patients into putative endotypes that are presumed to have a common underlying etiology. Obesity is known to create a proinflammatory state in similar chronic inflammatory conditions such as asthma. However, the potential impact of obesity in CRS has not been investigated.
METHODS: Samples were collected from 512 patients with CRS (235 CRSsNP, 277 CRSwNP) and 100 control patients undergoing surgery in a prospective longitudinal study. Mucus inflammatory cytokines were measured using a multiplex cytometric bead assay targeting IL-1a, IL-1b, IL-2, IL-3, IL-4, IL-5, IL-6, IL-7, IL-8, IL-9, IL-10, IL-11, IL-12, IL-13, IL-17, IL-18, IL-21, TNF-⍺, IFN-𝛾, eotaxin, RANTES, and GM-CSF. Cytokine levels were then compared between obese and non-obese patients using categorical and continuous measures of BMI.
RESULTS: In patients with CRSwNP, there were significant elevations in multiple pro-inflammatory cytokines. Levels of IL-2 (185 pg/mL vs. 39 pg/mL, p = 0.02), IL-4 (17.7 pg/mL vs. 6.3 pg/mL, p = 0.04), TNF-⍺ (58 pg/mL vs. 45 pg/mL, p = 0.04), IFN-ɣ (18.5 pg/mL vs. 17.3 pg/mL, p = 0.009), and GM-CSF (8.5 pg/mL vs. 2.5 pg/mL, p = 0.007) were elevated in obese CRSwNP patients. Continuous regression analysis did not confirm these results, potentially due to non-linear effects of obesity on sinonasal inflammation.
CONCLUSIONS: Obese CRSwNP patients have elevations in Type 1 and 2 cytokines compared to non-obese patients, potentially indicative of a pro-inflammatory bias in the sinonasal mucosa of obese patients. As such, there may be a role for weight loss and medical weight management in the treatment of CRSwNP, although further research is needed.