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鉴定饮食诱导的 2 型糖尿病小鼠模型中对伯克霍尔德氏菌假单胞菌感染的早期免疫反应缺陷。

Identification of defective early immune responses to Burkholderia pseudomallei infection in a diet-induced murine model of type 2 diabetes.

机构信息

College of Medicine and Dentistry, James Cook University, Queensland, 4811, Australia.

College of Public Health, Medical and Veterinary Sciences, James Cook University, Queensland, 4811, Australia.

出版信息

Microbes Infect. 2021 May-Jun;23(4-5):104793. doi: 10.1016/j.micinf.2021.104793. Epub 2021 Feb 8.

DOI:10.1016/j.micinf.2021.104793
PMID:33571673
Abstract

Co-occurrence of bacterial infections with type 2 diabetes (T2D) is a global problem. Melioidosis caused by Burkholderia pseudomallei is 10 times more likely to occur in patients with T2D, than in normoglycemic individuals. Using an experimental model of T2D, we observed that greater susceptibility in T2D was due to differences in proportions of infiltrating leucocytes and reduced levels of MCP-1, IFN-γ and IL-12 at sites of infection within 24 h post-infection. However, by 72 h the levels of inflammatory cytokines and bacteria were markedly higher in visceral tissue and blood in T2D mice. In T2D, dysregulated early immune responses are responsible for the greater predisposition to B. pseudomallei infection.

摘要

2 型糖尿病(T2D)合并细菌感染是一个全球性问题。比格氏杆菌引起的类鼻疽在 T2D 患者中的发生率比血糖正常个体高 10 倍。我们通过 T2D 实验模型发现,24 小时感染后,T2D 患者白细胞浸润比例差异和 MCP-1、IFN-γ 和 IL-12 水平降低导致 T2D 患者易感性增加。然而,72 小时时,T2D 小鼠内脏组织和血液中的炎症细胞因子和细菌水平明显升高。在 T2D 中,早期免疫反应失调导致对 B. pseudomallei 感染的易感性增加。

相似文献

1
Identification of defective early immune responses to Burkholderia pseudomallei infection in a diet-induced murine model of type 2 diabetes.鉴定饮食诱导的 2 型糖尿病小鼠模型中对伯克霍尔德氏菌假单胞菌感染的早期免疫反应缺陷。
Microbes Infect. 2021 May-Jun;23(4-5):104793. doi: 10.1016/j.micinf.2021.104793. Epub 2021 Feb 8.
2
Impaired early cytokine responses at the site of infection in a murine model of type 2 diabetes and melioidosis comorbidity.2 型糖尿病和类鼻疽合并症小鼠模型中感染部位早期细胞因子反应受损。
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Burkholderia pseudomallei triggers altered inflammatory profiles in a whole-blood model of type 2 diabetes-melioidosis comorbidity.类鼻疽伯克霍尔德菌在 2 型糖尿病-类鼻疽合并症的全血模型中引发改变的炎症特征。
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BpOmpW Antigen Stimulates the Necessary Protective T-Cell Responses Against Melioidosis.BpOmpW 抗原刺激针对类鼻疽病的必要保护性 T 细胞应答。
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Dysregulation of TNF-α and IFN-γ expression is a common host immune response in a chronically infected mouse model of melioidosis when comparing multiple human strains of Burkholderia pseudomallei.当比较多种人类布氏杆菌属假单胞菌菌株时,TNF-α和 IFN-γ表达失调是慢性感染小鼠模型中常见的宿主免疫反应。
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Altered macrophage function is associated with severe Burkholderia pseudomallei infection in a murine model of type 2 diabetes.巨噬细胞功能改变与 2 型糖尿病小鼠模型中严重伯克霍尔德菌假单胞菌感染有关。
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Reduced interleukin-17 expression of Burkholderia pseudomallei-infected peripheral blood mononuclear cells of diabetic patients.糖尿病患者感染伯克霍尔德菌后的外周血单个核细胞中白细胞介素-17表达降低。
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Delayed activation of host innate immune pathways in streptozotocin-induced diabetic hosts leads to more severe disease during infection with Burkholderia pseudomallei.链脲佐菌素诱导的糖尿病宿主中宿主固有免疫途径的延迟激活导致感染伯克霍尔德菌假单胞菌时疾病更严重。
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Regulatory role of GSK3β in the activation of NF-κB and modulation of cytokine levels in Burkholderia pseudomallei-infected PBMC isolated from streptozotocin-induced diabetic animals.GSK3β在从链脲佐菌素诱导的糖尿病动物分离的伯克霍尔德菌感染的外周血单核细胞中对NF-κB激活及细胞因子水平调节的调控作用
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