【摘要】 副猪嗜血杆菌(Hps)是猪上呼吸道常见条件致病菌之一,在临床上Hps和圆环病毒2型(PCV2)混合感染加剧了断奶仔猪多系统衰竭综合征的症状。为探讨Hps和PCV2共感染的致病机制,本试验建立了体外Hps和PCV2共感染猪肺泡巨噬细胞(PAM)的模型,分别检测感染12、24 h和36 h后的PAM细胞因子(IL-1β、TNF-α、IL-4和IL-10)、猪白细胞抗原(SLA)分子SLA-DR、SLA-DM以及共刺激分子CD80和CD86的mRNA转录水平,以探讨其动态变化规律。结果显示,与单一感染相比,Hps和PCV2共感染的PAM在感染24 h内,IL-1β和TNF-α表达水平显著上升(P<0.05),而IL-4和IL-10表达显著下降(P<0.05);在感染36 h内,CD80、CD86及SLA-DM、SLA-DR的表达水平显著下降(P<0.05)。结果表明,Hps和PCV2共感染增进了PAM促炎症因子表达,抑制了PAM抑炎因子表达及外源性抗原加工和递呈相关分子表达,从而消弱了其免疫功能。更多还原

【Abstract】 Haemophilus parasuis(Hps) is a common opportunistic pathogen of swine upper respiratory tract. In clinical setting, co-infection with Hps and porcine circovirus type 2(PCV2) exacerbates the symptoms of multiple system failure syndrome(PMWS) in weaned piglets. To study the pathogenic mechanism of Hps and PCV2 infections, co-infection with Hps and PCV2 was established in vitro using swine alveolar macrophages(PAM). The expression levels of PAM cytokines(IL-1β, TNF-α, IL-4 and IL-10), swine leukocyte antigen(SLA –DR, SLA-DM) and stimulating molecules CD80 and CD86 were detected using real time PCR at 12, 24 h and 36 h post infection(hpi). The results showed that compared with single infections, Hps and PCV2 co-infection significantly increased the expression levels of IL-1β and TNF-α(P < 0.05), but significantly decreased the expression levels of IL-4 and IL-10(P <0.05) within 24 hpi. Further, Hps and PCV2 co-infection significantly decreased the expression levels of CD80, CD86, SLA-DM and SLA-DR(P <0.05) within 36 hpi. Thus, by increasing the expression of proinflammatory factors, but inhibiting the expression of anti-inflammatory factors, the exogenous antigen processing and related molecules, Hps and PCV2 co-infection ultimately weakens the immune function of porcine alveolar macrophages.更多还原