鹦鹉热衣原体通过削弱鸡巨噬细胞的功能来触发H9N2禽流感病毒的入侵。,Animals

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鹦鹉热衣原体通过削弱鸡巨噬细胞的功能来触发H9N2禽流感病毒的入侵。
Animals ( IF 2.7 ) Pub Date : 2020-04-21 , DOI: 10.3390/ani10040722
Jun Chu _{1,

2} , Yongxia Guo ₃ , Guanlong Xu ₄ , Qiang Zhang ₃ , Zonghui Zuo ₃ , Qiang Li ₃ , Yihui Wang ₃ , Cheng He _{1,

3}

Affiliation

在一项先导研究中，同时感染鹦鹉热衣原体（C. psittaci）和H9N2病毒可导致20％的死亡率和严重的禽气管炎，为禽类呼吸道疾病的动物模型提供了依据。但是，其发病机理仍不清楚。在当前的研究中，我们假设C. psittaci感染执行巨噬细胞功能并促进H9N2感染。为了探索潜在的机制，我们研究了鹦鹉热衣原体和H9N2对同时感染鹦鹉热衣原体和H9N2的HD11细胞功能的影响。同时，我们仅使用鹦鹉热衣原体或H9N2感染作为对照组。结果表明，与与仅鹦鹉热衣原体或H9N2感染相比，鹦鹉热衣原体和H9N2可以显着加重HD11细胞的死亡率。此外，与C. psittaci和H9N2合并感染与单独的C. psittaci感染相比，在接种后12和24小时（hpi）不会诱导高C. psittaci负荷，但是与C. psittaci和H9N2合并感染可以增加在12 hpi时，HD11细胞中H9N2的负载与单独的H9N2相比。更重要的是，与C9 psittaci和H9N2共感染组相比，与H9N2或H9N2相比，诱导型一氧化氮合酶（iNOS）的表达水平，酶活性，一氧化氮（NO）产生和吞噬作用显着降低。在24 hpi时仅C. psittaci。最后，鹦鹉热衣原体感染诱导Th2型细胞因子白介素（IL）-4和IL-10的强表达，而干扰素γ（IFN-γ）和肿瘤坏死因子-α（TNF-α）与H9N2相比显着降低在感染后24 h独自感染。以上所有数据表明，鹦鹉热衣原体感染可通过损害巨噬细胞功能而促进H9N2侵袭并加重严重的禽气管炎。

"点击查看英文标题和摘要"

Chlamydia psittaci Triggers the Invasion of H9N2 Avian Influenza Virus by Impairing the Functions of Chicken Macrophages.

In a pilot study, simultaneous infection with Chlamydia psittaci (C. psittaci) and H9N2 virus induced 20% mortality and severe avian airsacculitis, shedding light on animal models of poultry respiratory diseases. However, the pathogenesis is still unclear. In the current study, we hypothesized that C. psittaci infection execrates macrophage function and facilitates H9N2 infection. To explore the potential mechanism, we studied the effect of C. psittaci and H9N2 on the functions of HD11 cells in vitro by simultaneous infection of C. psittaci and H9N2. At the same time, we used infection with C. psittaci or H9N2 alone as the control groups. The results showed that coinfection with C. psittaci and H9N2 could significantly aggravate the mortality of HD11 cells compared to C. psittaci or H9N2 infection alone. In addition, coinfection with C. psittaci and H9N2 did not induce high C. psittaci loads compared to C. psittaci infection alone at 12- and 24-hours post-inoculation (hpi), but coinfection with C. psittaci and H9N2 could increase the loads of H9N2 compared to H9N2 alone in HD11 cells at 12 hpi. More importantly, inducible nitric oxide synthase (iNOS) expression levels, enzyme activity, nitric oxide (NO) production, and phagocytosis were reduced significantly in the group with C. psittaci and H9N2 coinfection compared to those of H9N2 or C. psittaci alone at 24 hpi. Finally, C. psittaci infection induced robust expressions of type Th2 cytokines interleukin (IL)-4 and IL-10, while interferon gamma (IFN-γ) and tumor necrosis factor-α (TNF-α) displayed a significant decrease compared to H9N2 infection alone at 24 hpi. All the above data indicate that C. psittaci infection can facilitate H9N2 invasion and to aggravate severe avian airsacculitis by impairing macrophage functions.

更新日期：2020-04-21

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