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日本血吸虫肽 SJMHE1 抑制小鼠变应性哮喘的气道炎症。

Schistosoma japonicum peptide SJMHE1 suppresses airway inflammation of allergic asthma in mice.

机构信息

Department of Central Laboratory, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.

Department of Pediatrics, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.

出版信息

J Cell Mol Med. 2019 Nov;23(11):7819-7829. doi: 10.1111/jcmm.14661. Epub 2019 Sep 9.

DOI:10.1111/jcmm.14661
PMID:31496071
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6815837/
Abstract

Helminths and their products can shape immune responses by modulating immune cells, which are dysfunctional in inflammatory diseases such as asthma. We previously identified SJMHE1, a small molecule peptide from the HSP60 protein of Schistosoma japonicum. SJMHE1 can inhibit delayed-type hypersensitivity and collagen-induced arthritis in mice. In the present study, we evaluated this peptide's potential intervention effect and mechanism on ovalbumin-induced asthma in mice. SJMHE1 treatment suppressed airway inflammation in allergic mice, decreased the infiltrating inflammatory cells in the lungs and bronchoalveolar lavage fluid, modulated the production of pro-inflammatory and anti-inflammatory cytokines in the splenocytes and lungs of allergic mice, reduced the percentage of Th2 cells and increased the proportion of Th1 and regulatory T cells (Tregs). At the same time, Foxp3 and T-bet expression increased, and GATA3 and RORγt decreased in the lungs of allergic mice. We proved that SJMHE1 can interrupt the development of asthma by diminishing airway inflammation in mice. The down-regulation of Th2 response and the up-regulation of Th1 and Tregs response may contribute to the protection induced by SJMHE1 in allergic mice. SJMHE1 can serve as a novel therapy for asthma and other allergic or inflammatory diseases.

摘要

寄生虫及其产物可以通过调节免疫细胞来影响免疫反应,而免疫细胞在哮喘等炎症性疾病中功能失调。我们之前从日本血吸虫 HSP60 蛋白中鉴定出一种小分子肽 SJMHE1。SJMHE1 可以抑制小鼠迟发型超敏反应和胶原诱导性关节炎。在本研究中,我们评估了这种肽对卵清蛋白诱导的哮喘小鼠的潜在干预作用及其机制。SJMHE1 治疗抑制了过敏性小鼠的气道炎症,减少了肺部和支气管肺泡灌洗液中浸润的炎症细胞,调节了过敏性小鼠脾细胞和肺部促炎和抗炎细胞因子的产生,降低了 Th2 细胞的比例,增加了 Th1 和调节性 T 细胞(Tregs)的比例。同时,过敏性小鼠肺部的 Foxp3 和 T-bet 表达增加,GATA3 和 RORγt 减少。我们证明 SJMHE1 可以通过减少哮喘小鼠的气道炎症来阻断哮喘的发展。下调 Th2 反应和上调 Th1 和 Tregs 反应可能是 SJMHE1 诱导过敏性小鼠产生保护作用的原因。SJMHE1 可以作为哮喘和其他过敏性或炎症性疾病的一种新的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdca/6815837/ee1b791f4014/JCMM-23-7819-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdca/6815837/523c0706d2df/JCMM-23-7819-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdca/6815837/37d13c78c611/JCMM-23-7819-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdca/6815837/c69e44066aca/JCMM-23-7819-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdca/6815837/7b56d541f823/JCMM-23-7819-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdca/6815837/ee1b791f4014/JCMM-23-7819-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdca/6815837/523c0706d2df/JCMM-23-7819-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdca/6815837/37d13c78c611/JCMM-23-7819-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdca/6815837/c69e44066aca/JCMM-23-7819-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdca/6815837/7b56d541f823/JCMM-23-7819-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdca/6815837/ee1b791f4014/JCMM-23-7819-g006.jpg

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