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Modulation of chemokine and chemokine receptor expression following infection of porcine macrophages with African swine fever virus.

机译:猪巨噬细胞感染非洲猪瘟病毒后趋化因子和趋化因子受体表达的调节。

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African swine fever virus (ASFV) is the only member of the Asfarviridae, a large DNA virus family which replicates predominantly in the cytoplasm. Most isolates cause a fatal haemorrhagic disease in domestic pigs, although some low virulence isolates cause little or no mortality. The modulation of chemokine responses following infection of porcine macrophages with low and high virulence isolates was studied to indicate how this may be involved in the induction of pathogenesis and of effective immune responses. Infection with both low and high virulence isolates resulted in down-regulation of mRNA levels for chemokines CCL2, CCL3L, CXCL2 and chemokine receptors CCR1, CCR5, CXCR3, CXCR4 and up-regulation in expression of mRNAs for CCL4, CXCL10 and chemokine receptor CCR7. Levels of CCL4, CXCL8, CXCL10 mRNAs were higher in macrophages infected with low virulence isolate OURT88/3 compared to high virulence isolate Benin 97/1. Levels of CXCL8 and CCL2 protein were significantly reduced in supernatants from macrophages infected with Benin 97/1 isolate compared to OURT88/3 and mock-infected macrophages. There was also a decreased chemotactic response of donor cells exposed to supernatants from Benin 97/1 infected macrophages compared to those from OURT88/3 and mock-infected macrophages. The data show that infection of macrophages with the low virulence strain OURT88/3 induces higher expression of key inflammatory chemokines compared to infection with high virulence strain Benin 97/1. This may be important for the induction of effective protective immunity that has been observed in pigs immunised with the OURT88/3 isolate.
机译:非洲猪瘟病毒(ASFV)是Asfarviridae(大DNA病毒家族,主要在细胞质中复制)的唯一成员。尽管有些低毒力分离株几乎或根本没有引起死亡,但大多数分离株会在家猪中引起致命的出血性疾病。研究了用低毒力和高毒力分离株感染猪巨噬细胞后趋化因子反应的调节,以表明其可能如何参与发病机理和有效免疫反应的诱导。低毒力和高毒力分离物的感染均导致趋化因子CCL2,CCL3L,CXCL2和趋化因子受体CCR1,CCR5,CXCR3,CXCR4的mRNA水平下调,并导致CCL4,CXCL10和趋化因子受体CCR7的mRNA表达上调。与高毒力分离株贝宁97/1相比,在低毒力分离株OURT88 / 3感染的巨噬细胞中,CCL4,CXCL8,CXCL10 mRNA的水平更高。与OURT88 / 3和模拟感染的巨噬细胞相比,用贝宁97/1分离株感染的巨噬细胞的上清液中的CXCL8和CCL2蛋白水平显着降低。与来自OURT88 / 3和模拟感染的巨噬细胞相比,暴露于贝宁97/1感染的巨噬细胞上清液的供体细胞的趋化反应也有所降低。数据表明,与高毒力贝宁97/1感染相比,低毒力OURT88 / 3感染巨噬细胞诱导关键炎症趋化因子的更高表达。这对于诱导用OURT88 / 3分离株免疫的猪有效的保护性免疫可能很重要。

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