高密度脂蛋白在急性流感感染期间失去其抗炎性质
B J Van Lenten1, A C Wagner, D P Nayak
1Department of Medicine, UCLA School of Medicine, Los Angeles, California, USA. bvanlent@mednet.ucla.edu
Circulation
|May 23, 2001
概括
流感感染会改变高密度脂蛋白 (HDL) 的组成,降低其抗炎能力. 这项研究研究了小鼠在急性流感期间的HDL变化.
科学领域:
- 心血管科学 心血管科学
- 病毒学 病毒学
- 免疫学 免疫学 免疫学
背景情况:
- 病毒与动脉样硬化的发展有关.
- 流感病毒感染作为研究病毒对心血管健康影响的模型.
研究的目的:
- 为了研究急性流感感染对高密度脂蛋白 (HDL) 功能的影响.
- 为了确定流感如何影响HDL的抗atherogenic属性.
主要方法:
- C57BL/6J小鼠被内感染了流感A菌株WSN/33.
- 在感染后的不同时间点对高密度胆固醇成分 (偏氧酶,血小板激活因子乙,apoA-I,apoJ,血红) 和功能 (抑制低密度胆固醇氧化,单细胞化疗) 的分析.
- 测量血炎症标志物 (素-6,血清粉样蛋白A).测量血炎症标志物.
主要成果:
- 流感感染导致HDL中偏氧酶和血小板激活因子乙氨酸酶的活性下降.
- 高脂的抑制LDL氧化和单细胞化学反应的能力在感染后减少.
- 血中介质素-6和血清粉样蛋白A的水平增加,表明炎症反应.
结论:
- 急性流感感染会改变HDL的组成,特别是影响偏氧酶,血小板激活因子乙,血红和apoJ水平.
- 这些高密度胆固醇 (HDL) 变化导致其抗炎性质丧失.
- 流感引起的HDL变化可能会导致动脉动脉产生.
相关概念视频
Inflammation
46.6K
Overview
46.6K
Influenza
87
Influenza is an acute, highly communicable viral disease that affects the respiratory tract and is responsible for seasonal epidemics worldwide. Influenza A is the most prevalent type associated with widespread outbreaks and is subtyped based on two surface glycoproteins: hemagglutinin (H) and neuraminidase (N), as in H1N1. These glycoproteins are essential for viral infectivity, transmission, and immune recognition. Transmission occurs primarily through respiratory droplets and contaminated...
87
Inhibitors of Viral Protein Synthesis
58
Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
58
Acute Inflammation I: Inflammatory Response
94
Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect...
94
Acute Inflammation I: Cellular Phase
82
The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...
82
Acute Inflammation II: Local and Systemic Effects
56
Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
56


