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血清白细胞介素-1β可作为重度持续性变应性鼻炎患儿的生物标志物。

Serum IL-1β can be a biomarker in children with severe persistent allergic rhinitis.

作者信息

Han Myung Woul, Kim Song Hee, Oh Inbo, Kim Yang Ho, Lee Jiho

机构信息

1Department of Otolaryngology, Ulsan University Hospital, University of Ulsan College of Medicine, 877 Bangeojinsunhwan-doro, Dong-gu, Ulsan, 44033 Republic of Korea.

2Environmental Health Center, University of Ulsan College of Medicine, Ulsan, Republic of Korea.

出版信息

Allergy Asthma Clin Immunol. 2019 Sep 18;15:58. doi: 10.1186/s13223-019-0368-8. eCollection 2019.

DOI:10.1186/s13223-019-0368-8
PMID:31548841
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6749717/
Abstract

BACKGROUND

Allergic rhinitis (AR) is one of the most common diseases globally and usually persists throughout life. In the present study, we aimed to determine whether the expression of inflammatory biomarkers has a relationship with the severity of allergic rhinitis and with comorbid asthma or other allergic diseases in children.

METHODS

For diagnosis of AR, the skin prick test was performed to measure the responses to 18 allergens. Blood levels of eosinophils and immunoglobulin E (IgE) were examined. We classified the patients into 2 groups based on the severity of the condition as Group 1 [intermittent AR (IAR) or mild persistent AR (PAR)] and Group 2 (moderate to severe PAR). To determine the expression of inflammatory biomarkers, in serum and several biomarkers (caspase-1, IL-1β, CCL-11, CCL-24 and IL-33) were measured in the serum using enzyme-linked immunosorbent assay (ELISA). Additionally, we analyzed the correlation between clinical variables and the expression of biomarkers (eosinophils count, IL-1β and CCL-24) and the severity of AR.

RESULTS

We found that eosinophils count, IL-1β, a marker of activation of inflammasomes, and CCL-24 were significantly increased in the moderate to severe PAR group ( = 0.008,  = 0.003,  = 0.039). Additionally, the expressions of eosinophil count, IL-1β and CCL-24 were significantly higher in patients with active asthmatic symptoms than in those without these conditions. On univariate analysis, allergic rhinitis in sibling, paternal allergic rhinitis, high expression of eosinophils count, IL-1β and CCL-24, history of active asthma and atopy correlated with severity of AR. Multivariate analysis showed only paternal allergic rhinitis and high expression of IL-1β as significant risk factors of moderate to severe PAR with 6.4 fold and 4.7 fold-increase in risk, respectively ( = 0.011 and  = 0.030).

CONCLUSION

In conclusion, this study provides the first evidence that an excessive release of biologically active IL-1β may promote inflammation in severe PAR. It demonstrates that IL-1β can be a biomarker for active allergic diseases such as AR, asthma, and atopy. Moreover, this finding suggests that IL-1B should be investigated as a therapeutic target in severe PAR and other allergic diseases.

摘要

背景

变应性鼻炎(AR)是全球最常见的疾病之一,通常会持续终生。在本研究中,我们旨在确定炎症生物标志物的表达是否与儿童变应性鼻炎的严重程度以及合并哮喘或其他过敏性疾病有关。

方法

为诊断AR,进行皮肤点刺试验以测量对18种变应原的反应。检测嗜酸性粒细胞和免疫球蛋白E(IgE)的血液水平。我们根据病情严重程度将患者分为两组,即第1组[间歇性AR(IAR)或轻度持续性AR(PAR)]和第2组(中度至重度PAR)。为确定炎症生物标志物的表达,使用酶联免疫吸附测定(ELISA)检测血清中的几种生物标志物(半胱天冬酶-1、IL-1β、CCL-11、CCL-24和IL-33)。此外,我们分析了临床变量与生物标志物(嗜酸性粒细胞计数、IL-1β和CCL-24)的表达以及AR严重程度之间的相关性。

结果

我们发现,中度至重度PAR组中嗜酸性粒细胞计数、IL-1β(一种炎性小体激活标志物)和CCL-24显著升高(P = 0.008,P = 0.003,P = 0.039)。此外,有活动性哮喘症状的患者中嗜酸性粒细胞计数、IL-1β和CCL-24的表达显著高于无这些症状的患者。单因素分析显示,同胞患变应性鼻炎、父亲患变应性鼻炎、嗜酸性粒细胞计数、IL-1β和CCL-24的高表达、活动性哮喘病史和特应性与AR的严重程度相关。多因素分析显示,只有父亲患变应性鼻炎和IL-1β的高表达是中度至重度PAR的显著危险因素,风险分别增加6.4倍和4.7倍(P = 0.011和P = 0.030)。

结论

总之,本研究提供了首个证据,即生物活性IL-1β的过度释放可能会促进重度PAR中的炎症。它表明IL-1β可以作为AR、哮喘和特应性等活动性过敏性疾病的生物标志物。此外,这一发现表明应将IL-1B作为重度PAR和其他过敏性疾病的治疗靶点进行研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc56/6749717/c88404cf157d/13223_2019_368_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc56/6749717/78f2bbe7a44a/13223_2019_368_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc56/6749717/c88404cf157d/13223_2019_368_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc56/6749717/78f2bbe7a44a/13223_2019_368_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fc56/6749717/c88404cf157d/13223_2019_368_Fig2_HTML.jpg

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