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猫传染性腹膜炎作为一种全身性炎症性疾病:肝脏和心脏对发病机制的贡献。

Feline Infectious Peritonitis as a Systemic Inflammatory Disease: Contribution of Liver and Heart to the Pathogenesis.

机构信息

Institute of Veterinary Pathology, Vetsuisse Faculty, University of Zurich, 8057 Zurich, Switzerland.

Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, 8057 Zurich, Switzerland.

出版信息

Viruses. 2019 Dec 10;11(12):1144. doi: 10.3390/v11121144.

Abstract

Feline infectious peritonitis (FIP) is a fatal immune-mediated disease of cats, induced by feline coronavirus (FCoV). A combination of as yet poorly understood host and viral factors combine to cause a minority of FCoV-infected cats to develop FIP. Clinicopathological features include fever, vasculitis, and serositis, with or without effusions; all of which indicate a pro-inflammatory state with cytokine release. As a result, primary immune organs, as well as circulating leukocytes, have thus far been of most interest in previous studies to determine the likely sources of these cytokines. Results have suggested that these tissues alone may not be sufficient to induce the observed inflammation. The current study therefore focussed on the liver and heart, organs with a demonstrated ability to produce cytokines and therefore with huge potential to exacerbate inflammatory processes. The IL-12:IL-10 ratio, a marker of the immune system's inflammatory balance, was skewed towards the pro-inflammatory IL-12 in the liver of cats with FIP. Both organs were found to upregulate mRNA expression of the inflammatory triad of cytokines IL-1β, IL-6, and TNF-α in FIP. This amplifying step may be one of the missing links in the pathogenesis of this enigmatic disease.

摘要

猫传染性腹膜炎(FIP)是一种由猫冠状病毒(FCoV)引起的猫致命免疫介导性疾病。目前仍不清楚一些宿主和病毒因素的组合如何导致少数 FCoV 感染的猫发生 FIP。临床病理特征包括发热、血管炎和浆膜炎,伴有或不伴有渗出液;所有这些都表明存在细胞因子释放的促炎状态。因此,在以前的研究中,主要的免疫器官以及循环白细胞一直是确定这些细胞因子可能来源的最感兴趣的对象。结果表明,仅这些组织可能不足以诱导观察到的炎症。因此,目前的研究集中在肝脏和心脏上,这两个器官具有产生细胞因子的能力,因此具有加剧炎症过程的巨大潜力。IL-12:IL-10 比值是免疫系统炎症平衡的标志物,在患有 FIP 的猫的肝脏中,该比值偏向于促炎的 IL-12。研究发现,这两个器官在 FIP 中均上调了炎症三联体细胞因子 IL-1β、IL-6 和 TNF-α 的 mRNA 表达。这一放大步骤可能是这种神秘疾病发病机制中的缺失环节之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/148e/6949997/0c0ec817e075/viruses-11-01144-g001.jpg

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