ALV-J strain SCAU-HN06 induces innate immune responses in chicken primary monocyte-derived macrophages.

ALV-J strain SCAU-HN06 induces innate immune responses in chicken primary monocyte-derived macrophages.
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ALV-J菌株SCAU-HN06诱导鸡原代单核细胞衍生的巨噬细胞的先天免疫反应

DOI:
10.3382/ps/pew229
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发表时间:
2017-01-01
期刊:
影响因子:
4.4
通讯作者:
Zhang X
Zhang X
中科院分区:
农林科学2区
文献类型:
--
作者:
Feng M;Dai M;Cao W;Tan Y;Li Z;Shi M;Zhang X

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J亚群禽白血病病毒(ALV-J)可引起鸡的终生感染,并可逃避宿主的免疫防御。鉴于巨噬细胞在宿主先天免疫中作为抵御病原体入侵的重要防线,本研究对鸡原代单核细胞来源的巨噬细胞(MDM)感染ALV-J后的功能和先天免疫应答进行了研究。结果表明,ALV-J在MDM细胞中稳定存在,但病毒的生长速度明显低于在DF-1细胞中的生长速度。我们还发现,ALV-J感染显著增加了一氧化氮(NO)的产生,但对MDM的吞噬能力没有影响。有趣的是,感染ALV-J的MDM细胞在感染早期迅速促进粘病毒耐药性1(Mx)(3小时、6小时)、ISG12(6小时)和白介素1β(IL-1β)(3小时、12小时)的表达,而在感染后期则显著降低Mx(24小时、36小时)、ISG12(36小时)的表达,而对IL-1β(24小时、36小时)的产生几乎没有影响。感染ALV-J的MDM细胞在感染后3h至36h,干扰素-β(干扰素-β)和白介素6(IL-6)的蛋白水平显著升高。感染ALV-J的MDM细胞在感染36 h后,IL-10蛋白水平显著降低。这些结果表明ALV-J能够诱导宿主的先天免疫反应,我们推测巨噬细胞在宿主先天免疫攻击和ALV-J免疫逃逸中起重要作用。
Avian leucosis virus subgroup J (ALV-J) can cause lifelong infection and can escape from the host immune defenses in chickens. Since macrophages act as the important defense line against invading pathogens in host innate immunity, we investigated the function and innate immune responses of chicken primary monocyte-derived macrophages (MDM) after ALV-J infection in this study. Our results indicated that ALV-J was stably maintained in MDM cells but that the viral growth rate was significantly lower than that in DF-1 cells. We also found that ALV-J infection significantly increased nitric oxide (NO) production, but had no effect on MDM phagocytic capacity. Interestingly, infection with ALV-J rapidly promoted the expression levels of Myxovirus resistance 1 (Mx) (3 h, 6 h), ISG12 (6 h), and interleukin-1β (IL-1β) (3 h, 12 h) at an early infection stage, whereas it sharply decreased the expression of Mx (24 h, 36 h), ISG12 (36 h), and made little change on IL-1β (24 h, 36 h) production at a late infection stage in MDM cells. Moreover, the protein levels of interferon-β (IFN-β) and interleukin-6 (IL-6) had sharply increased in infected MDM cells from 3 to 36 h post infection (hpi) of ALV-J. And, the protein level of interleukin-10 (IL-10) was dramatically decreased at 36 hpi in MDM cells infected with ALV-J. These results demonstrate that ALV-J can induce host innate immune responses and we hypothesize that macrophages play an important role in host innate immune attack and ALV-J immune escape.
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