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细胞外 DNA 与化学诱导的结肠炎小鼠的肠道炎症相关。

Extracellular DNA Correlates with Intestinal Inflammation in Chemically Induced Colitis in Mice.

机构信息

Institute of Molecular Biomedicine, Faculty of Medicine, Comenius University in Bratislava, 81108 Bratislava, Slovakia.

Institute of Physiology, Faculty of Medicine, Comenius University in Bratislava, 81372 Bratislava, Slovakia.

出版信息

Cells. 2021 Jan 6;10(1):81. doi: 10.3390/cells10010081.

DOI:10.3390/cells10010081
PMID:33418977
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7825321/
Abstract

Circulating extracellular DNA (ecDNA) is known to worsen the outcome of many diseases. ecDNA released from neutrophils during infection or inflammation is present in the form of neutrophil extracellular traps (NETs). It has been shown that higher ecDNA concentration occurs in a number of inflammatory diseases including inflammatory bowel disease (IBD). Enzymes such as peptidyl arginine deiminases (PADs) are crucial for NET formation. We sought to describe the dynamics of ecDNA concentrations and fragmentation, along with NETosis during a mouse model of chemically induced colitis. Plasma ecDNA concentration was highest on day seven of dextran sulfate sodium (DSS) intake and the increase was time-dependent. This increase correlated with the percentage of cells undergoing NETosis and other markers of disease activity. Relative proportion of nuclear ecDNA increased towards more severe colitis; however, absolute amount decreased. In colon explant medium, the highest concentration of ecDNA was on day three of DSS consumption. Early administration of PAD4 inhibitors did not alleviate disease activity, but lowered the ecDNA concentration. These results uncover the biological characteristics of ecDNA in IBD and support the role of ecDNA in intestinal inflammation. The therapeutic intervention aimed at NETs and/or nuclear ecDNA has yet to be fully investigated.

摘要

循环细胞外 DNA（ecDNA）已知会使许多疾病的预后恶化。中性粒细胞在感染或炎症期间释放的 ecDNA 以中性粒细胞细胞外陷阱（NETs）的形式存在。已经表明，在包括炎症性肠病（IBD）在内的许多炎症性疾病中，ecDNA 浓度更高。肽基精氨酸脱亚氨酶（PADs）等酶对于 NET 的形成至关重要。我们试图描述在化学诱导结肠炎的小鼠模型中，ecDNA 浓度和片段化以及 NETosis 的动态变化。在葡聚糖硫酸钠（DSS）摄入的第 7 天，血浆 ecDNA 浓度最高，并且这种增加是时间依赖性的。这种增加与细胞发生 NETosis 的百分比以及其他疾病活动标志物相关。核 ecDNA 的相对比例随着结肠炎的加重而增加；然而，绝对数量减少。在结肠外植体培养基中，DSS 消耗的第 3 天 ecDNA 浓度最高。早期给予 PAD4 抑制剂不能缓解疾病活动，但降低了 ecDNA 浓度。这些结果揭示了 IBD 中 ecDNA 的生物学特征，并支持 ecDNA 在肠道炎症中的作用。针对 NETs 和/或核 ecDNA 的治疗干预尚未得到充分研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/4f3ac5ba297c/cells-10-00081-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/373f7e3594a0/cells-10-00081-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/7520cd836526/cells-10-00081-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/a3bc9870b20f/cells-10-00081-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/00cf8749103c/cells-10-00081-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/2263e9973af3/cells-10-00081-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/efaff8db0b18/cells-10-00081-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/89e80c23a974/cells-10-00081-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/e8dd749e7145/cells-10-00081-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/4f3ac5ba297c/cells-10-00081-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/373f7e3594a0/cells-10-00081-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/7520cd836526/cells-10-00081-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/a3bc9870b20f/cells-10-00081-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/00cf8749103c/cells-10-00081-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/2263e9973af3/cells-10-00081-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/efaff8db0b18/cells-10-00081-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/89e80c23a974/cells-10-00081-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/e8dd749e7145/cells-10-00081-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/254c/7825321/4f3ac5ba297c/cells-10-00081-g009.jpg

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