Feng Min, Dai Manman, Cao Weisheng, Tan Yan, Li Zhenhui, Shi Meiqing, Zhang Xiquan
Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou 510642, Guangdong, China.
Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding and Key Laboratory of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, Guangzhou 510642, Guangdong, China.
Poult Sci. 2017 Jan 1;96(1):42-50. doi: 10.3382/ps/pew229. Epub 2016 Aug 2.
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.
禽白血病病毒J亚群（ALV-J）可引起终身感染，并能逃避鸡的宿主免疫防御。由于巨噬细胞在宿主固有免疫中作为抵御入侵病原体的重要防线，因此在本研究中我们调查了鸡原代单核细胞衍生巨噬细胞（MDM）在感染ALV-J后的功能和固有免疫反应。我们的结果表明，ALV-J在MDM细胞中稳定维持，但病毒生长速率显著低于DF-1细胞。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，在感染早期，ALV-J感染迅速促进了抗黏液病毒1（Mx）（3小时、6小时）、ISG12（6小时）和白细胞介素-1β（IL-1β）（3小时、12小时）的表达水平，而在感染后期，它急剧降低了MDM细胞中Mx（24小时、36小时）、ISG12（36小时）的表达，并且对IL-1β（24小时、36小时）的产生影响不大。此外，在感染ALV-J后3至36小时，感染的MDM细胞中干扰素-β（IFN-β）和白细胞介素-6（IL-6）的蛋白水平急剧增加。并且，在感染ALV-J 的MDM细胞中，白细胞介素-10（IL-10）的蛋白水平在感染后36小时显著降低。这些结果表明，ALV-J可诱导宿主固有免疫反应，我们推测巨噬细胞在宿主固有免疫攻击和ALV-J免疫逃逸中起重要作用。
