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抑制尿酸或白细胞介素-1β可改善呼吸道合胞病毒免疫病理学及哮喘的发展。

Inhibition of uric acid or IL-1β ameliorates respiratory syncytial virus immunopathology and development of asthma.

作者信息

Schuler Charles F, Malinczak Carrie-Anne, Best Shannon K K, Morris Susan B, Rasky Andrew J, Ptaschinski Catherine, Lukacs Nicholas W, Fonseca Wendy

机构信息

Division of Allergy and Clinical Immunology, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.

Mary H. Weiser Food Allergy Center, University of Michigan, Ann Arbor, MI, USA.

出版信息

Allergy. 2020 Sep;75(9):2279-2293. doi: 10.1111/all.14310. Epub 2020 May 15.

DOI:10.1111/all.14310
PMID:32277487
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7494620/
Abstract

BACKGROUND

Respiratory syncytial virus (RSV) affects most infants early in life and is associated with increased asthma risk. The specific mechanism remains unknown.

OBJECTIVE

To investigate the role of uric acid (UA) and IL-1β in RSV immunopathology and asthma predisposition.

METHODS

Tracheal aspirates from human infants with and without RSV were collected and analyzed for pro-IL-1β mRNA and protein to establish a correlation in human disease. Neonatal mouse models of RSV were employed, wherein mice infected at 6-7 days of life were analyzed at 8 days postinfection, 5 weeks postinfection, or after a chronic cockroach allergen asthma model. A xanthine oxidase inhibitor or IL-1 receptor antagonist was administered during RSV infection.

RESULTS

Human tracheal aspirates from RSV-infected infants showed elevated pro-IL-1β mRNA and protein. Inhibition of UA or IL-1β during neonatal murine RSV infection decreased mucus production, reduced cellular infiltrates to the lung (especially ILC2s), and decreased type 2 immune responses. Inhibition of either UA or IL-1β during RSV infection led to chronic reductions in pulmonary immune cell composition and reduced type 2 immune responses and reduced similar responses after challenge with cockroach antigen.

CONCLUSIONS

Inhibiting UA and IL-1β during RSV infection ameliorates RSV immunopathology, reduces the consequences of allergen-induced asthma, and presents new therapeutic targets to reduce early-life viral-induced asthma development.

摘要

背景

呼吸道合胞病毒（RSV）在大多数婴儿生命早期感染，并与哮喘风险增加相关。具体机制尚不清楚。

目的

研究尿酸（UA）和白细胞介素-1β（IL-1β）在RSV免疫病理学和哮喘易感性中的作用。

方法

收集有或无RSV感染的人类婴儿的气管吸出物，分析前白细胞介素-1β的mRNA和蛋白质，以建立与人类疾病的相关性。采用RSV新生小鼠模型，对出生6-7天感染的小鼠在感染后8天、感染后5周或在慢性蟑螂变应原哮喘模型后进行分析。在RSV感染期间给予黄嘌呤氧化酶抑制剂或白细胞介素-1受体拮抗剂。

结果

RSV感染婴儿的人类气管吸出物显示前白细胞介素-1β的mRNA和蛋白质升高。新生小鼠RSV感染期间抑制UA或IL-1β可减少黏液产生，减少肺部细胞浸润（尤其是2型固有淋巴细胞），并降低2型免疫反应。RSV感染期间抑制UA或IL-1β均可导致肺部免疫细胞组成长期减少，降低2型免疫反应，并减少蟑螂抗原激发后的类似反应。

结论

RSV感染期间抑制UA和IL-1β可改善RSV免疫病理学，减轻变应原诱导的哮喘后果，并为减少生命早期病毒诱导的哮喘发展提供新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98c3/7494620/082dd3a664d5/nihms-1590999-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98c3/7494620/8b06b207731a/nihms-1590999-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98c3/7494620/9285c228342b/nihms-1590999-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98c3/7494620/bd364a0c8d1d/nihms-1590999-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98c3/7494620/63d509f830c2/nihms-1590999-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98c3/7494620/03b965557f36/nihms-1590999-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98c3/7494620/082dd3a664d5/nihms-1590999-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98c3/7494620/8b06b207731a/nihms-1590999-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98c3/7494620/9285c228342b/nihms-1590999-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98c3/7494620/bd364a0c8d1d/nihms-1590999-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98c3/7494620/63d509f830c2/nihms-1590999-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98c3/7494620/03b965557f36/nihms-1590999-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98c3/7494620/082dd3a664d5/nihms-1590999-f0006.jpg

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