CAJ | 학술논문

通过PCV2与PPV混合感染猪肺泡巨噬细胞,探讨PCV2与PPV体外混合感染的致病机制。体外分离猪肺泡巨噬细胞( PAMs),分为PCV2、PPV、PCV2/PPV混合感染组和对照组,采用实时荧光定量PCR技术检测PAMs中PCV2与PPV病毒拷贝数及细胞因子IFN-γ、TNF-α和IL-10的mRNA转录水平的变化。结果表明,PPV能在PAMs中增殖,而PCV2在肺泡巨噬细胞中增殖效率较低；PCV2能促进PPV增殖；PPV单独感染PAMs后能促进IFN-γ和TNF-α的表达；PCV2单独感染PAMs后能促进IFN-γ的表达,并在感染早期促进TNF-α的表达；PCV2与PPV混合感染后能显著抑制IFN-γ的表达,在感染早期对TNF-α的促进作用高于PCV2单独感染组,并能短暂的刺激IL-10的过量表达。说明PCV2与PPV混合感染存在协同致病作用,两种病毒共同刺激了TNF-α和IL-10的大量表达,抑制了IFN-γ的表达。
통과PCV2여PPV혼합감염저폐포거서세포,탐토PCV2여PPV체외혼합감염적치병궤제。체외분리저폐포거서세포( PAMs),분위PCV2、PPV、PCV2/PPV혼합감염조화대조조,채용실시형광정량PCR기술검측PAMs중PCV2여PPV병독고패수급세포인자IFN-γ、TNF-α화IL-10적mRNA전록수평적변화。결과표명,PPV능재PAMs중증식,이PCV2재폐포거서세포중증식효솔교저；PCV2능촉진PPV증식；PPV단독감염PAMs후능촉진IFN-γ화TNF-α적표체；PCV2단독감염PAMs후능촉진IFN-γ적표체,병재감염조기촉진TNF-α적표체；PCV2여PPV혼합감염후능현저억제IFN-γ적표체,재감염조기대TNF-α적촉진작용고우PCV2단독감염조,병능단잠적자격IL-10적과량표체。설명PCV2여PPV혼합감염존재협동치병작용,량충병독공동자격료TNF-α화IL-10적대량표체,억제료IFN-γ적표체。
This study was to define the pathogenesis of coinfection of porcine cirvovirus type 2(PCV2) and porcine parvovirus( PPV ) in vitro. Porcine alveolar macrophages ( PAMs) were isolated, and divided into PCV2 infection group, PPV infection group, PCV2/PPV coinfection group and control group. PCV2 and PPV nucleic acid, and mR-NA levels of cytokines IFN-γ, TNF-α and IL-10 in PAMs were detected by realtime-PCR. The results showed that PPV could proliferate in PAMs, but the proliferation effi-ciency for PCV2 was low. PCV2 infection increased the expressions of IFN-γ mRNA and TNF-α mRNA expres-sion, PCV2/PPV coinfection lowered the expression level of IFN-γ mRNA. However, the level of TNF-α in PCV2/PPV coinfection group was higher than that in PCV2 group during early infection,and a transient IL-10 increasing was detected as well. These results suggested that the suppression of IFN-γand over-expression of TNF-αand IL-10 caused by PCV2/PPV coinfection might contribute to the inhibition of cellular immunity.