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在 A/J 小鼠中感染早期的细胞因子谱。

Cytokine Profile in Early Infection by in A/J Mice.

机构信息

Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo Zip code 05508-900, Brazil.

Institute of Tropical Medicine, University of São Paulo, São Paulo Zip code 05403-000, Brazil.

出版信息

J Immunol Res. 2019 Oct 7;2019:1892508. doi: 10.1155/2019/1892508. eCollection 2019.

Abstract

Leptospirosis is considered a neglected disease with an estimated more than one million cases every year. Since rodents are at the same time the main reservoir and generally asymptomatic to infection, understanding why some animal species are resistant and others are susceptible to this infection would shed some light in how to control this important zoonosis. The innate immune response against is mainly dependent on phagocytosis and activation of the Complement System. In this context, cytokines may drive the early control of infection and the adaptive response. Since the Complement System is important to eliminate leptospires , we investigated if Complement C5 in A/J mice would modulate the cytokine production during infection by serovar Kennewicki type Pomona Fromm (LPF). Thus, our aim was to investigate the systemic levels of pro- and anti-inflammatory cytokines during infection in the blood, liver, lung, and kidney on the third and sixth days of infection in A/J C5 and A/J C5 mice. Blood levels of TNF-, IL-6, IFN-, and MCP-1 reached a peak on the third day. Although both mouse strains developed splenomegaly, similar histopathological alterations in the liver and the lung, levels of pro- and anti-inflammatory cytokines were different. A/J C5 mice had higher levels of liver IL-10, IL-1, IL-12p40, and IL-12p70 and kidney IL-1, IL-12p40, and IL-12p70 on the sixth day of infection when compared to A/J C5 mice. Our results showed that in A/J genetic background, the Complement component C5 modulates a cytokine profile in the liver and kidney of infected mice, which may play a role in the control of disease progression.

摘要

钩端螺旋体病被认为是一种被忽视的疾病,估计每年有超过 100 万例。由于啮齿动物既是主要的储存宿主,而且通常对感染无症状,因此了解为什么有些动物物种对这种感染具有抗性,而另一些动物则易感染,这将有助于我们控制这种重要的人畜共患病。对的固有免疫反应主要依赖于吞噬作用和补体系统的激活。在这种情况下,细胞因子可能会驱动感染的早期控制和适应性反应。由于补体系统对于消除钩端螺旋体至关重要,我们研究了 A/J 小鼠中的补体 C5 是否会在感染时调节细胞因子的产生由血清型肯纳威克氏菌 Pomona Fromm (LPF)引起。因此,我们的目的是研究感染期间血液、肝脏、肺和肾脏中促炎和抗炎细胞因子的全身水平在感染的第 3 和第 6 天 A/J C5 和 A/J C5 小鼠。TNF-、IL-6、IFN-和 MCP-1 的血液水平在第 3 天达到峰值。尽管两种小鼠品系均发生了脾肿大,但肝脏和肺部的组织病理学改变相似,促炎和抗炎细胞因子的水平不同。与 A/J C5 小鼠相比,A/J C5 小鼠在感染的第 6 天肝脏中具有更高水平的 IL-10、IL-1、IL-12p40 和 IL-12p70,以及肾脏中的 IL-1、IL-12p40 和 IL-12p70。我们的结果表明,在 A/J 遗传背景下,补体成分 C5 调节感染小鼠肝脏和肾脏中的细胞因子谱,这可能在控制疾病进展中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8091/6800925/551896403e1d/JIR2019-1892508.001.jpg

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