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首页> 外文期刊>Infection and immunity >Host-Pathogen Interactions of Actinobacillus pleuropneumoniae with Porcine Lung and Tracheal Epithelial Cells
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Host-Pathogen Interactions of Actinobacillus pleuropneumoniae with Porcine Lung and Tracheal Epithelial Cells

机译：胸膜肺炎放线杆菌与猪肺和气管上皮细胞的宿主病原体相互作用

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Host-pathogen interactions are of great importance in understanding the pathogenesis of infectious microorganisms. We developed in vitro models to study the host-pathogen interactions of porcine respiratory tract pathogens using two immortalized epithelial cell lines, namely, the newborn pig trachea (NPTr) and St. Jude porcine lung (SJPL) cell lines. We first studied the interactions of Actinobacillus pleuropneumoniae, an important swine pathogen, using these models. Under conditions where cytotoxicity was absent or low, we showed that A. pleuropneumoniae adheres to both cell lines, stimulating the induction of NF-κB. The NPTr cells consequently secrete interleukin 8, while the SJPL cells do not, since they are deprived of the NF-κB p65 subunit. Cell death ultimately occurs by necrosis, not apoptosis. The transcriptomic profile of A. pleuropneumoniae was determined after contact with the porcine lung epithelial cells by using DNA microarrays. Genes such as tadB and rcpA, members of a putative adhesin locus, and a gene whose product has high homology to the Hsf autotransporter adhesin of Haemophilus influenzae were upregulated, as were the genes pgaBC, involved in biofilm biosynthesis, while capsular polysaccharide-associated genes were downregulated. The in vitro models also proved to be efficient with other swine pathogens, such as Actinobacillus suis, Haemophilus parasuis, and Pasteurella multocida. Our results demonstrate that interactions of A. pleuropneumoniae with host epithelial cells seem to involve complex cross talk which results in regulation of various bacterial genes, including some coding for putative adhesins. Furthermore, our data demonstrate the potential of these in vitro models in studying the host-pathogen interactions of other porcine respiratory tract pathogens.
机译：宿主-病原体的相互作用在理解传染性微生物的发病机理中非常重要。我们开发了体外模型，以使用两种永生化上皮细胞系，即新生猪气管（NPTr）和圣裘德猪肺（SJPL）细胞系研究猪呼吸道病原体的宿主-病原体相互作用。我们首先使用这些模型研究了重要的猪病原体胸膜肺炎放线杆菌的相互作用。在没有或没有细胞毒性的条件下，我们证明了 A。胸膜肺炎粘附在两种细胞系上，刺激了NF-κB的诱导。 NPTr细胞因此分泌白介素8，而SJPL细胞则不分泌白介素8，因为它们被剥夺了NF-κBp65亚基。细胞死亡最终通过坏死而不是凋亡发生。 A的转录组谱。用DNA芯片检测猪肺上皮细胞后测定胸膜肺炎。 tadB 和 rcpA 等基因，是假定的粘附素基因座的成员，其产物与流感嗜血杆菌的Hsf自转运粘附素具有高度同源性的基因>被上调，而 pgaBC 基因也参与生物膜生物合成，而荚膜多糖相关基因被下调。体外模型还被证明对其他猪病原体有效，例如 Actinobacillus suis ， Haemophilus parasuis 和 Pasteurella multocida 。我们的结果证明了 A的相互作用。带有宿主上皮细胞的胸膜肺炎似乎涉及复杂的串扰，导致多种细菌基因的调控，包括一些假定的粘附素编码。此外，我们的数据证明了这些体外模型在研究其他猪呼吸道病原体的宿主-病原体相互作用中的潜力。

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