瑞索尔D2是一种强大的白细胞调节剂,可以控制微生物败血症
Matthew Spite1, Lucy V Norling, Lisa Summers
1Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Nature
|October 30, 2009
概括
瑞索尔文D2 (RvD2) 通过减少中性粒细胞迁移和细菌负载,积极解决炎症. 这种脂质调解剂通过促进免疫解决和警,提高了败血症模型中的生存率.
科学领域:
- 免疫学 免疫学 免疫学
- 生物化学 生物化学
- 药理学 药理学是指药理学的学科.
背景情况:
- 炎症解消是一个活跃的,复杂的过程.
- 溶解素是调节疾病衰退 (catabasis) 的脂质媒介.
- 在此之前,Resolvin D2 (RvD2) 在解决方案中的具体作用尚不清楚.
研究的目的:
- 阐明RvD2.2的特定的解决功能.
- 研究RvD2在减少过度炎症方面的机制.
- 评估RvD2在诸如败血症之类的炎症状况中的治疗潜力.
主要方法:
- 在体内研究RvD2对中性粒细胞贩运和白细胞-内皮细胞相互作用的影响.
- 给RvD2的小鼠进行了多微生物性败血症诱导的结和穿刺 (CLP).
- 评估RvD2对细菌负担,细胞因子产生,免疫细胞招募和巨细胞消化作用的影响.
主要成果:
- RvD2显示出强大的立体选择性减少中性粒细胞向炎症部位的迁移.
- RvD2通过氧化的产生减少了白细胞-内皮细胞相互作用,并改变了粘附受体表达.
- 在CLP诱导的败血症中,RvD2降低了细菌负载,细胞因子水平和中性粒细胞的招募,同时增强了巨细胞灭菌.
- 在败血症模型中,RvD2治疗显著增加了生存率.
结论:
- RvD2是过度炎症反应的强有力的内源调节剂.
- RvD2通过多个细胞点起作用,刺激炎症.
- RvD2保持免疫警,同时促进解决,为败血症和其他炎症性疾病提供治疗潜力.
相关概念视频
01:28Inflammatory Response
An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
01:24T Cell Types and Functions
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
01:28Regulation of Bacterial Virulence
Pathogenic bacteria employ a range of regulatory mechanisms to modulate the expression of virulence genes in response to environmental and host-derived signals. These mechanisms ensure that virulence factors are expressed only under favorable conditions, thereby optimizing infection and survival strategies.Mechanisms of Virulence RegulationKey regulatory strategies include:Two-Component Systems: These consist of a membrane-bound sensor kinase and a cytoplasmic response regulator. Environmental...
01:26Acute Inflammation I: Inflammatory Response
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 damage-associated...
01:26Acute Inflammation II: Cellular Phase
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...
01:25Acute Inflammation III: Local and Systemic Effects
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...