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肠炎沙门氏菌和海德堡沙门氏菌感染鸡巨噬细胞样细胞期间诱导的磷酸化依赖性差异信号传导和葡萄糖免疫代谢反应

The Differential Phosphorylation-Dependent Signaling and Glucose Immunometabolic Responses Induced during Infection by Enteritidis and Heidelberg in Chicken Macrophage-like cells.

作者信息

Perry Famatta, Johnson Casey, Aylward Bridget, Arsenault Ryan J

机构信息

Department of Animal and Food Sciences, University of Delaware, Newark, DE 19716, USA.

出版信息

Microorganisms. 2020 Jul 14;8(7):1041. doi: 10.3390/microorganisms8071041.

DOI:10.3390/microorganisms8071041
PMID:32674261
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7409154/
Abstract

is a burden to the poultry, health, and food safety industries, resulting in illnesses, food contamination, and recalls. subspecies Enteritidis ( Enteritidis) is one of the most prevalent serotypes isolated from poultry. subspecies Heidelberg ( Heidelberg), which is becoming as prevalent as Enteritidis, is one of the five most isolated serotypes. Although Enteritidis and Heidelberg are almost genetically identical, they both are capable of inducing different immune and metabolic responses in host cells to successfully establish an infection. Therefore, using the kinome peptide array, we demonstrated that Enteritidis and Heidelberg infections induced differential phosphorylation of peptides on Rho proteins, caspases, toll-like receptors, and other proteins involved in metabolic- and immune-related signaling of HD11 chicken macrophages. Metabolic flux assays measuring extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) demonstrated that Enteritidis at 30 min postinfection (p.i.) increased glucose metabolism, while Heidelberg at 30 min p.i. decreased glucose metabolism. Enteritidis is more invasive than Heidelberg. These results show different immunometabolic responses of HD11 macrophages to Enteritidis and Heidelberg infections.

摘要

这对家禽、健康和食品安全行业来说是一种负担,会导致疾病、食品污染和召回。肠炎沙门氏菌肠炎亚种(Enteritidis)是从家禽中分离出的最常见血清型之一。海德堡沙门氏菌亚种(Heidelberg)正变得与肠炎沙门氏菌一样普遍,是最常分离出的五种血清型之一。尽管肠炎沙门氏菌和海德堡沙门氏菌在基因上几乎相同,但它们都能够在宿主细胞中诱导不同的免疫和代谢反应,从而成功建立感染。因此,我们使用激酶组肽阵列证明,肠炎沙门氏菌和海德堡沙门氏菌感染会诱导HD11鸡巨噬细胞中Rho蛋白、半胱天冬酶、Toll样受体以及其他参与代谢和免疫相关信号传导的蛋白质上的肽发生差异磷酸化。测量细胞外酸化率(ECAR)和氧消耗率(OCR)的代谢通量分析表明,感染后30分钟(p.i.)的肠炎沙门氏菌会增加葡萄糖代谢,而感染后30分钟的海德堡沙门氏菌会降低葡萄糖代谢。肠炎沙门氏菌比海德堡沙门氏菌更具侵袭性。这些结果显示了HD11巨噬细胞对肠炎沙门氏菌和海德堡沙门氏菌感染的不同免疫代谢反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e4/7409154/c7b4b15fb898/microorganisms-08-01041-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e4/7409154/d9ee0575fe41/microorganisms-08-01041-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e4/7409154/c7b4b15fb898/microorganisms-08-01041-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e4/7409154/d9ee0575fe41/microorganisms-08-01041-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/62e4/7409154/c7b4b15fb898/microorganisms-08-01041-g002.jpg

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