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A1-40 寡聚物通过 TLR4 和 NADPH 氧化酶依赖的途径在年龄相关性黄斑变性中触发中性粒细胞细胞外陷阱形成。

A1-40 Oligomers Trigger Neutrophil Extracellular Trap Formation through TLR4- and NADPH Oxidase-Dependent Pathways in Age-Related Macular Degeneration.

机构信息

Department of Ophthalmology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Chongqing Key Laboratory of Ophthalmology, Chongqing Eye Institute, Chongqing, China.

出版信息

Oxid Med Cell Longev. 2022 Jun 18;2022:6489923. doi: 10.1155/2022/6489923. eCollection 2022.

DOI:10.1155/2022/6489923
PMID:35761872
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9233592/
Abstract

Neutrophils participate in the advancement of the human innate immune system and respond to perceived endogenous and exogenous threats. As a response mechanism, neutrophil extracellular traps (NETs) form near pathogens and surrounding tissues during an immune response. Drusen is an important marker of Age-Related Macular Degeneration (AMD) and plays an important role in the course of AMD. A1-40 is the main component of drusen. However, the relationship between NETs and AMD or A1-40 is unclear. Here, we found elevated levels of NETs in the serum of AMD patients and elevated levels in the serum of mouse models. We also observed the accumulation of neutrophils in the mouse retina. In addition, the production of NETs was inhibited by PAD4 inhibitors, which can alleviate chronic inflammation. Moreover, we confirmed that A1-40 can induce NETs formation via the Toll-like receptor 4 (TLR4) and neutrophil NADPH oxidase (NOX) pathways. Our study confirmed that the formation of NETs is induced by A1-40, and the results suggest that NETs may play a vital role in AMD pathogenesis.

摘要

中性粒细胞参与人体先天免疫系统的发展，并对感知到的内源性和外源性威胁做出反应。作为一种反应机制，中性粒细胞胞外诱捕网（NETs）在免疫反应期间在病原体和周围组织附近形成。 沉积物是年龄相关性黄斑变性（AMD）的重要标志物，并在 AMD 的病程中起重要作用。 A1-40 是沉积物的主要成分。然而，NETs 与 AMD 或 A1-40 之间的关系尚不清楚。在这里，我们发现 AMD 患者的血清中 NETs 水平升高，并且在小鼠模型的血清中也升高。我们还观察到中性粒细胞在小鼠视网膜中的积累。此外，通过 PAD4 抑制剂抑制 NETs 的产生，可以减轻慢性炎症。此外，我们证实 A1-40 可以通过 Toll 样受体 4（TLR4）和中性粒细胞 NADPH 氧化酶（NOX）途径诱导 NETs 的形成。我们的研究证实 A1-40 诱导 NETs 的形成，这表明 NETs 在 AMD 的发病机制中可能起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/173a/9233592/1fa73c48467d/OMCL2022-6489923.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/173a/9233592/d54b92e4d5c8/OMCL2022-6489923.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/173a/9233592/95113cc5ca53/OMCL2022-6489923.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/173a/9233592/95ab4d97bc9b/OMCL2022-6489923.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/173a/9233592/d3b613cccf75/OMCL2022-6489923.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/173a/9233592/1fa73c48467d/OMCL2022-6489923.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/173a/9233592/d54b92e4d5c8/OMCL2022-6489923.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/173a/9233592/48e40ee1fa2c/OMCL2022-6489923.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/173a/9233592/43e3fca299c0/OMCL2022-6489923.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/173a/9233592/95113cc5ca53/OMCL2022-6489923.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/173a/9233592/95ab4d97bc9b/OMCL2022-6489923.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/173a/9233592/d3b613cccf75/OMCL2022-6489923.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/173a/9233592/1fa73c48467d/OMCL2022-6489923.007.jpg

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