首页> 美国卫生研究院文献>Poultry Science >ALV-J strain SCAU-HN06 induces innate immune responses in chicken primary monocyte-derived macrophages
【2h】

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

机译:ALV-J株SCAU-HN06在鸡原代单核细胞衍生的巨噬细胞中诱导先天免疫应答

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

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.
机译:禽白血病病毒亚类J(ALV-J)可以引起终生感染,并且可以逃避宿主的免疫防御。由于巨噬细胞是抵御宿主先天免疫中入侵病原体的重要防御线,因此在这项研究中,我们调查了鸡原代单核细胞衍生巨噬细胞(MDM)的功能和先天免疫反应。我们的结果表明,ALV-J在MDM细胞中稳定维持,但病毒生长速度明显低于DF-1细胞。我们还发现,ALV-J感染显着增加了一氧化氮(NO)的产生,但对MDM吞噬能力没有影响。有趣的是,ALV-J感染迅速促进了粘液病毒抗性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)的表达水平在MDM感染后期,它在感染的早期阶段显着降低了Mx(24 h,36 h),ISG12(36 h)的表达,并且对IL-1β(24 h,36 h)产生的变化很小细胞。此外,在感染的MDM细胞中,从ALV-J感染后(hpi)的3小时到36小时,干扰素β(IFN-β)和白介素6(IL-6)的蛋白质水平急剧增加。并且,在感染了ALV-J的MDM细胞中,白细胞介素10(IL-10)的蛋白水平在36hpi时显着降低。这些结果表明,ALV-J可以诱导宿主先天性免疫应答,我们假设巨噬细胞在宿主先天性免疫攻击和ALV-J免疫逃逸中起重要作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号