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脂多糖通过激活TLR4-MAPK-NF-κB/AP-1信号通路诱导肉鸡雏鸡急性法氏囊萎缩。

Lipopolysaccharide induces acute bursal atrophy in broiler chicks by activating TLR4-MAPK-NF-κB/AP-1 signaling.

作者信息

Ansari Abdur Rahman, Li Ning-Ya, Sun Zhi-Jian, Huang Hai-Bo, Zhao Xing, Cui Lei, Hu Ya-Fang, Zhong Ju-Ming, Karrow Niel A, Liu Hua-Zhen

机构信息

Department of Basic Veterinary Medicine, College of Animal Science and Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, China.

Department of Basic Sciences, Section of Anatomy and Histology, College of Veterinary and Animal Sciences (CVAS) Jhang, University of Veterinary and Animal Sciences (UVAS), Lahore, Pakistan.

出版信息

Oncotarget. 2017 Aug 5;8(65):108375-108391. doi: 10.18632/oncotarget.19964. eCollection 2017 Dec 12.

DOI:10.18632/oncotarget.19964
PMID:29312537
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5752450/
Abstract

We investigated the mechanisms that induce atrophy of the chicken bursa of Fabricius (BF) upon lipopolysaccharide (LPS) treatment in young chicks. LPS treatment resulted in ∼36% decrease in bursal weight within 36 h ( < 0.01). Histological analysis showed infiltration of eosinophilic heterophils and nucleated oval shaped RBCs in or near blood vessels of the BF from LPS-treated chicks. Scanning electron micrographs showed severe erosion and breaks in the mucosal membrane at 12 h and complete exuviation of bursal mucosal epithelial cells at 36 h. We observed decreased cell proliferation (low PCNA positivity) and increased apoptosis (high TUNEL and ssDNA positivity) in the BF 12-72 h after LPS treatment. RNA-seq analysis of the BF transcriptome showed 736 differentially expressed genes with most expression changes (637/736) 12 h after LPS treatment. KEGG pathway analysis identified TLR4-MAPK-NF-κB/AP-1 as the key signaling pathway affected in response to LPS stimulation. These findings indicate LPS activates the TLR4-MAPK-NF-κB/AP-1 signaling pathway that mediates acute atrophy of the chicken bursa of Fabricius by inducing inflammation and apoptosis.

摘要

我们研究了幼雏经脂多糖(LPS)处理后诱导法氏囊(BF)萎缩的机制。LPS处理导致36小时内法氏囊重量下降约36%(P<0.01)。组织学分析显示,LPS处理雏鸡的BF血管内或血管附近有嗜酸性异嗜性粒细胞和有核椭圆形红细胞浸润。扫描电子显微镜照片显示,12小时时粘膜出现严重侵蚀和破损,36小时时法氏囊粘膜上皮细胞完全脱落。我们观察到LPS处理后12 - 72小时,BF中的细胞增殖减少(PCNA阳性率低),凋亡增加(TUNEL和单链DNA阳性率高)。BF转录组的RNA测序分析显示有736个差异表达基因,其中大多数表达变化(637/736)发生在LPS处理后12小时。KEGG通路分析确定TLR4-MAPK-NF-κB/AP-1是受LPS刺激影响的关键信号通路。这些发现表明,LPS激活TLR4-MAPK-NF-κB/AP-1信号通路,通过诱导炎症和凋亡介导雏鸡法氏囊的急性萎缩。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23e7/5752450/1290307f85d9/oncotarget-08-108375-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23e7/5752450/fa6389289366/oncotarget-08-108375-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23e7/5752450/cba3be9d788b/oncotarget-08-108375-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23e7/5752450/303337d9fdbb/oncotarget-08-108375-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23e7/5752450/235527fe8f96/oncotarget-08-108375-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23e7/5752450/69657cfa0bed/oncotarget-08-108375-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23e7/5752450/1290307f85d9/oncotarget-08-108375-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23e7/5752450/fa6389289366/oncotarget-08-108375-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23e7/5752450/cba3be9d788b/oncotarget-08-108375-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23e7/5752450/303337d9fdbb/oncotarget-08-108375-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23e7/5752450/235527fe8f96/oncotarget-08-108375-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23e7/5752450/69657cfa0bed/oncotarget-08-108375-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23e7/5752450/1290307f85d9/oncotarget-08-108375-g006.jpg

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