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

机译:脂多糖通过激活TLR4-MAPK-NF-κB/ AP-1信号传导诱导肉鸡急性法氏囊萎缩

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摘要

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 (P < 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.
机译:我们调查了在幼雏中脂多糖(LPS)处理后诱导Fabricius鸡法氏囊(BF)萎缩的机制。 LPS处理可使法氏囊重量在36小时内降低约36%(P <0.01)。组织学分析显示,LPS处理的雏鸡的嗜酸性嗜异性细胞和有核的椭圆形红细胞在BF的血管中或附近渗透。扫描电子显微镜照片显示,在12 h时,黏膜严重腐蚀和破裂,在36 h时,囊性黏膜上皮细胞完全消失。我们观察到LPS处理后的BF 12-72 h,细胞增殖减少(PCNA阳性低)和凋亡增加(TUNEL和ssDNA阳性高)。 LPS处理后12 h,BF转录组的RNA-seq分析显示了736个差异表达基因,其表达变化最多(637/736)。 KEGG通路分析确定TLR4-MAPK-NF-κB/ AP-1是响应LPS刺激而受影响的关键信号通路。这些发现表明,LPS激活TLR4-MAPK-NF-κB/ AP-1信号传导途径,该途径通过诱导炎症和细胞凋亡来介导法氏囊属鸡法氏囊的急性萎缩。

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