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Understanding Haemophilus parasuis infection in porcine spleen through a transcriptomics approach

机译:通过转录组学方法了解猪脾副猪嗜血杆菌感染

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Background Haemophilus parasuis (HPS) is an important swine pathogen that causes Gl?sser's disease, which is characterized by fibrinous polyserositis, meningitis and arthritis. The molecular mechanisms that underlie the pathogenesis of the disease remain poorly understood, particularly the resistance of porcine immune system to HPS invasion. In this study, we investigated the global changes in gene expression in the spleen following HPS infection using the Affymetrix Porcine Genechip?. Results A total of 931 differentially expressed (DE) transcripts were identified in the porcine spleen 7 days after HPS infection; of these, 92 unique genes showed differential expression patterns based on analysis using BLASTX and Gene Ontology. The DE genes involved in the immune response included genes for inflammasomes (RETN, S100A8, S100A9, S100A12), adhesion molecules (CLDN3, CSPG2, CD44, LGALS8), transcription factors (ZBTB16, SLC39A14, CEBPD, CEBPB), acute-phase proteins and complement (SAA1, LTF, HP, C3), differentiation genes for epithelial cells and keratinocytes (TGM1, MS4A8B, CSTA), and genes related to antigen processing and presentation (HLA-B, HLA-DRB1). Further immunostimulation analyses indicated that mRNA levels of S100A8, S100A9, and S100A12 in porcine PK-15 cells increased within 48 h and were sustained after administration of lipopolysaccharide (LPS) and Poly(I:C) respectively. In addition, mapping of DE genes to porcine health traits QTL regions showed that 70 genes were distributed in 7 different known porcine QTL regions. Finally, 10 DE genes were validated by quantitative PCR. Conclusion Our findings demonstrate previously unrecognized changes in gene transcription that are associated with HPS infection in vivo, and many potential cascades identified in the study clearly merit further investigation. Our data provide new clues to the nature of the immune response in mammals, and we have identified candidate genes that are related to resistance to HPS.
机译:背景副猪嗜血杆菌(HPS)是一种重要的猪病原体,可引起格塞尔病,该病的特征是纤维性多发性浆膜炎,脑膜炎和关节炎。对该病发病机理的分子机制仍知之甚少,特别是猪免疫系统对HPS入侵的抵抗力。在这项研究中,我们调查了使用Affymetrix Porcine基因芯片在HPS感染后脾脏中基因表达的总体变化。结果HPS感染7天后,在猪脾中共鉴定出931个差异表达(DE)转录本。其中,有92个独特基因根据BLASTX和Gene Ontology的分析显示出差异表达模式。参与免疫应答的DE基因包括炎性体(RETN,S100A8,S100A9,S100A12),粘附分子(CLDN3,CSPG2,CD44,LGALS8),转录因子(ZBTB16,SLC39A14,CEBPD,CEBPB),急性期蛋白和补体(SAA1,LTF,HP,C3),上皮细胞和角质形成细胞的分化基因(TGM1,MS4A8B,CSTA),以及与抗原加工和呈递相关的基因(HLA-B,HLA-DRB1)。进一步的免疫刺激分析表明,猪PK-15细胞中S100A8,S100A9和S100A12的mRNA水平在48小时内增加,并分别在给予脂多糖(LPS)和聚(I:C)后得以维持。另外,将DE基因映射到猪健康性状QTL区域显示70个基因分布在7个不同的已知猪QTL区域中。最后,通过定量PCR验证了10个DE基因。结论我们的发现表明,以前体内与HPS感染相关的基因转录尚无法识别,并且该研究中鉴定出的许多潜在级联显然值得进一步研究。我们的数据为哺乳动物免疫应答的性质提供了新的线索,并且我们已经鉴定出与抗HPS相关的候选基因。

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