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严重的乳房裂伤性皮炎病变转录组学表明,皮肤屏障受损、伤口修复缺陷和炎症反应失调是发病机制中的关键因素。

Severe udder cleft dermatitis lesion transcriptomics points to an impaired skin barrier, defective wound repair and a dysregulated inflammatory response as key elements in the pathogenesis.

机构信息

Department of Internal Medicine, Reproduction and Population Medicine, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium.

Laboratory of Pharmaceutical Biotechnology, Faculty of Pharmaceutical Sciences, Ghent University, Ghent, Belgium.

出版信息

PLoS One. 2023 Jul 24;18(7):e0288347. doi: 10.1371/journal.pone.0288347. eCollection 2023.

DOI:10.1371/journal.pone.0288347
PMID:37486897
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10365316/
Abstract

This study is the first to investigate the transcriptomic changes occurring in severe udder cleft dermatitis lesions (UCD) in Holstein-Friesian cows. An examination of the gene expression levels in natural UCD lesions and healthy udder skin through RNA Seq-Technology provided a deeper insight into the inflammatory pathways associated with this disease. A clear distinction between the gene expression patterns of UCD lesions and healthy skin was shown in the principal component analysis. Genes coding for inflammatory molecules were upregulated such as the chemokines C-X-C motif ligand 2 (CXCL2), 5 (CXCL5) and 8 (CXCL8), and C-C motif ligand 11 (CCL11). Moreover, the genes coding for the multifunctional molecules ADAM12 and SLPI were amongst the highest upregulated ones, whereas the most downregulated genes included the ones coding for keratins and keratin-associated molecules. Predominantly inflammatory pathways such as the chemokine signaling, cytokine receptor interaction and IL-17 signaling pathway were significantly upregulated in the pathway analysis. These results point towards a fulminant, dysregulated inflammatory response concomitant with a disruption of the skin barrier integrity and a hampered wound repair mechanism in severe UCD lesions.

摘要

本研究首次调查了荷斯坦弗里森奶牛严重乳房皲裂性皮炎(UCD)病变中的转录组变化。通过 RNA Seq 技术检查天然 UCD 病变和健康乳房皮肤中的基因表达水平,深入了解了与该疾病相关的炎症途径。主成分分析显示 UCD 病变和健康皮肤的基因表达模式明显不同。编码炎症分子的基因上调,如趋化因子 C-X-C 基序配体 2(CXCL2)、5(CXCL5)和 8(CXCL8)以及 C-C 基序配体 11(CCL11)。此外,多功能分子 ADAM12 和 SLPI 的编码基因也属于上调表达最高的基因之一,而下调表达最明显的基因包括角蛋白和角蛋白相关分子的编码基因。通路分析显示,趋化因子信号转导、细胞因子受体相互作用和 IL-17 信号通路等主要炎症途径明显上调。这些结果表明,在严重的 UCD 病变中,存在着剧烈的、失调的炎症反应,同时伴随着皮肤屏障完整性的破坏和伤口修复机制的受阻。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644e/10365316/76cdf59c3c81/pone.0288347.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644e/10365316/1f0b622a8028/pone.0288347.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644e/10365316/76cdf59c3c81/pone.0288347.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644e/10365316/1f0b622a8028/pone.0288347.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/644e/10365316/76cdf59c3c81/pone.0288347.g002.jpg

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