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群 V 分泌型磷脂酶 A2 在 Th2 细胞因子和树突状细胞驱动的气道高反应性和重塑中的关键作用。

Key role of group v secreted phospholipase A2 in Th2 cytokine and dendritic cell-driven airway hyperresponsiveness and remodeling.

机构信息

Center for Allergy and Inflammation, UW Medicine at South Lake Union, Department of Medicine, University of Washington, Seattle, Washington, United States of America.

出版信息

PLoS One. 2013;8(2):e56172. doi: 10.1371/journal.pone.0056172. Epub 2013 Feb 25.

DOI:10.1371/journal.pone.0056172
PMID:23451035
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3581544/
Abstract

BACKGROUND

Previous work has shown that disruption of the gene for group X secreted phospholipase A2 (sPLA2-X) markedly diminishes airway hyperresponsiveness and remodeling in a mouse asthma model. With the large number of additional sPLA2s in the mammalian genome, the involvement of other sPLA2s in the asthma model is possible - in particular, the group V sPLA2 (sPLA2-V) that like sPLA2-X is highly active at hydrolyzing membranes of mammalian cells.

METHODOLOGY AND PRINCIPAL FINDINGS

The allergen-driven asthma phenotype was significantly reduced in sPLA2-V-deficient mice but to a lesser extent than observed previously in sPLA2-X-deficient mice. The most striking difference observed between the sPLA2-V and sPLA2-X knockouts was the significant impairment of the primary immune response to the allergen ovalbumin (OVA) in the sPLA2-V(-/-) mice. The impairment in eicosanoid generation and dendritic cell activation in sPLA2-V(-/-) mice diminishes Th2 cytokine responses in the airways.

CONCLUSIONS

This paper illustrates the diverse roles of sPLA2s in the immunopathogenesis of the asthma phenotype and directs attention to developing specific inhibitors of sPLA2-V as a potential new therapy to treat asthma and other allergic disorders.

摘要

背景

先前的研究表明，X 组分泌型磷脂酶 A2（sPLA2-X）基因的破坏显著降低了小鼠哮喘模型中的气道高反应性和重塑。由于哺乳动物基因组中存在大量其他的 sPLA2s，其他 sPLA2s 可能参与了哮喘模型 - 特别是具有高度水解哺乳动物细胞膜活性的 V 组 sPLA2（sPLA2-V）。

方法和主要发现

在 sPLA2-V 缺陷型小鼠中，过敏原驱动的哮喘表型显著降低，但程度低于先前在 sPLA2-X 缺陷型小鼠中观察到的。在 sPLA2-V 和 sPLA2-X 敲除小鼠之间观察到的最显著差异是 sPLA2-V(-/-) 小鼠对过敏原卵清蛋白（OVA）的初次免疫反应显著受损。sPLA2-V(-/-) 小鼠中花生四烯酸生成和树突状细胞激活的受损，降低了气道中的 Th2 细胞因子反应。

结论

本文说明了 sPLA2s 在哮喘表型的免疫发病机制中的多种作用，并将注意力集中于开发 sPLA2-V 的特异性抑制剂，作为治疗哮喘和其他过敏疾病的潜在新疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25d9/3581544/01a81349df58/pone.0056172.g013.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25d9/3581544/01147d12b99b/pone.0056172.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25d9/3581544/94508e37982e/pone.0056172.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/25d9/3581544/6d46d0b5a644/pone.0056172.g010.jpg
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