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首页> 外文期刊>Veterinary Microbiology >Induction of innate host responses characterized by production of interleukin (IL)-1 beta and recruitment of macrophages to the respiratory tract of chickens following infection with infectious bronchitis virus (IBV)
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Induction of innate host responses characterized by production of interleukin (IL)-1 beta and recruitment of macrophages to the respiratory tract of chickens following infection with infectious bronchitis virus (IBV)

机译：在用传染性支气管炎病毒感染后，诱导白细胞介素（IL）-1β（IL）-1β和急血栓呼吸道呼吸道的泌尿外宿主反应诱导

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Infectious bronchitis virus (IBV) infection is a major cause of economic losses to the poultry industry. Due to limitations in current control measures, alternative approaches, based on thorough understanding of the host responses are required. As one of the key component of the avian immune system, the innate immune system has a crucial role in limiting virus replication at the initial stage of the infection. As parts of the innate host response, macrophages and cytokines, such as interleukin (IL)-1 beta, are critical components as shown in other host-virus infection models. Since information on the importance of macrophages and IL-1 beta in IBV infection in chickens is limited, our objective was to determine the association of IL-1 beta, originating from avian macrophages and IBV infection in the trachea and lung. Following experimental IBV infection in 6 days old chickens, we found increased production of IL-1 beta and increased recruitment of macrophages in the respiratory tract. Towards the end of the study (5 and 7 days following the IBV infection), the recruited macrophages appear to be a significant source IL-1 beta. However, only the recruitment of macrophages in the lung correlated with IBV genome loads in this tissue. In conclusion, the present study demonstrates that recruitment of macrophages and the production of IL-1 beta originating from macrophages, as well as other sources, occur following IBV infection in the respiratory tract suggesting potential roles of these mediators in the host responses to IBV infection. However, further studies are warranted to elucidate whether macrophages and IL-1 beta are the causes of reduced IBV genome loads in the respiratory tract and also to investigate whether immune mediators that were not measured in the current study were involved in reducing IBV genome load in the respiratory tract towards the end of the study.
机译：感染性支气管炎病毒（IBV）感染是家禽业经济损失的主要原因。由于当前控制措施的限制，需要基于对彻底了解主机响应的替代方法。作为禽类免疫系统的关键组成部分之一，先天免疫系统在限制感染初始阶段限制病毒复制方面具有至关重要的作用。作为先天宿主响应，巨噬细胞和细胞因子的部分，例如白细胞介素（IL）-1β，是其他宿主病毒感染模型所示的关键组分。由于有关鸡巨噬细胞和IL-1β的重要性的信息有限，因此我们的目的是确定IL-1β的关联，来自气管和肺的禽类巨噬细胞和IBV感染。在6天老鼠的实验性IBV感染之后，我们发现增加了IL-1β的产量并增加了呼吸道中巨噬细胞的募集。在研究结束时（IBV感染后5和7天），募集的巨噬细胞似乎是一个重要的IL-1 Beta。然而，只有这种组织中的肺中巨噬细胞的募集与IBV基因组载荷相关。总之，本研究表明，在IBV感染在对IBV感染中的潜在作用的潜在作用后，发生巨噬细胞的募集和源自巨噬细胞的IL-1β的产生，以及其他来源的促进巨噬细胞和其他来源的产生。然而，有必要进一步研究来阐明巨噬细胞和IL-1β是否是呼吸道中IBV基因组载荷减少的原因，并且还研究在目前研究中未测量的免疫介质是否参与降低IBV基因组载荷呼吸道在研究结束时。

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