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基质金属蛋白酶-2 在过敏性支气管哮喘中的保护作用。

Protective Role of Matrix Metalloproteinase-2 in Allergic Bronchial Asthma.

机构信息

Department of Pulmonary and Critical Care Medicine, Mie University Graduate School of Medicine, Tsu, Japan.

Department of Immunology, Mie University Graduate School of Medicine, Tsu, Japan.

出版信息

Front Immunol. 2019 Aug 2;10:1795. doi: 10.3389/fimmu.2019.01795. eCollection 2019.

DOI:10.3389/fimmu.2019.01795
PMID:31428095
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6687911/
Abstract

Inflammation, reversible obstruction, and hyperresponsiveness of the airways are characteristic findings of bronchial asthma. Several evidence has demonstrated the involvement of matrix metalloproteinase-2 in allergic airway inflammation. Matrix metalloproteinase-2 may promote aberrant tissue remodeling in late stages of allergic airway inflammation. However, whether matrix metalloproteinase-2 is detrimental or protective in early stages of allergic airway inflammation remains unclear. To evaluate this here we compared the severity of allergic bronchial asthma between mice overexpressing human matrix metalloproteinase-2 and wild type mice. After sensitization and challenge with an allergen, mice overexpressing the human matrix metalloproteinase-2 showed a significant reduction in airway hyperresponsiveness and in the expression of Th2 cytokines and IgE compared to their wild type counterparts. An inhibitor of matrix metalloproteinases abolished this beneficial effect of human matrix metalloproteinase-2 overexpression. Allergen-sensitized and challenged human matrix metalloproteinase-2 transgenic mice had enhanced percentage of M1 macrophages with increased expression of inducible nitric oxide synthase and STAT1 activation in the lungs compared to their wild type counterparts. There was no difference in the percentage of regulatory T cells between mouse groups. The results of this study showed that matrix metalloproteinase-2 is protective in allergic bronchial asthma by promoting polarization of macrophages to M1 phenotype.

摘要

气道炎症、可逆性阻塞和高反应性是支气管哮喘的特征性表现。有几项证据表明基质金属蛋白酶-2参与了过敏性气道炎症。基质金属蛋白酶-2可能促进过敏性气道炎症晚期的异常组织重塑。然而，基质金属蛋白酶-2在过敏性气道炎症的早期阶段是有害的还是保护性的尚不清楚。为了评估这一点，我们比较了过表达人基质金属蛋白酶-2的小鼠和野生型小鼠之间过敏性支气管哮喘的严重程度。在过敏原致敏和攻击后，与野生型相比，过表达人基质金属蛋白酶-2的小鼠气道高反应性和 Th2 细胞因子及 IgE 的表达显著降低。基质金属蛋白酶抑制剂消除了人基质金属蛋白酶-2过表达的这种有益作用。与野生型相比，过敏原致敏和攻击的人基质金属蛋白酶-2转基因小鼠的 M1 巨噬细胞百分比增加，诱导型一氧化氮合酶表达增加，STAT1 激活增加。两组小鼠之间调节性 T 细胞的百分比没有差异。这项研究的结果表明，基质金属蛋白酶-2通过促进巨噬细胞向 M1 表型极化而在过敏性支气管哮喘中起保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/8e400113ba31/fimmu-10-01795-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/69be6a55f338/fimmu-10-01795-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/204f29ab614c/fimmu-10-01795-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/59c42c803286/fimmu-10-01795-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/f458e7bff957/fimmu-10-01795-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/43f2bef36a70/fimmu-10-01795-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/9b00769256a0/fimmu-10-01795-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/8e400113ba31/fimmu-10-01795-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/69be6a55f338/fimmu-10-01795-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/204f29ab614c/fimmu-10-01795-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/59c42c803286/fimmu-10-01795-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/f458e7bff957/fimmu-10-01795-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/43f2bef36a70/fimmu-10-01795-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/9b00769256a0/fimmu-10-01795-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6687911/8e400113ba31/fimmu-10-01795-g0007.jpg

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