雌激醇和孕激素在血管损伤后差异调节白细胞透
Dongqi Xing1, Andrew Miller, Lea Novak
1Vascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, UAB Station, Birmingham, AL 35294, USA. dqxing@uab.edu
Circulation
|December 31, 2003
概括
雌激素 (E2) 减少炎症细胞的迁移,如粒细胞,进入受伤的老鼠动脉. 甲 (MPA) 阻断了这种保护作用,突出了E2.
科学领域:
- 血管生物学 血管生物学
- 内分泌学 在内分泌学.
- 免疫学 免疫学 免疫学
背景情况:
- 在血管损伤反应中,炎症至关重要.
- 雌激素 (17β-雌激醇,E2) 抑制了新内的形成.
- 麦德罗西孕酸 (MPA) 抵消了E2的抑制作用.
研究的目的:
- 为了调查E2是否抑制炎症细胞在受伤后迁移到老鼠动脉.
- 为了确定MPA是否阻断E2对炎症细胞迁移的影响.
主要方法:
- 经过卵巢切除的老鼠接受了E2,MPA,E2+MPA,或车辆,其次是气球冠状动脉损伤.
- 炎症细胞群 (粒细胞,单细胞/巨细胞,T淋巴细胞) 通过流动细胞计量在受伤后的1,3,7天量化.
- 免疫组织化学证实了细胞局部化.
主要成果:
- 与对照人群相比,受伤的动脉显示颗粒细胞,单细胞/巨细胞和T淋巴细胞的显著增加.
- E2治疗减少了大约50%的颗粒细胞和单细胞/巨细胞种群,并增加了T淋巴细胞.
- 单独的MPA没有作用,但完全阻止了E2对炎症细胞的抑制作用.
结论:
- 通过减少白细胞进入受损血管,E2可能会限制新极端反应.
- 白细胞从冒险性/周冒险性组织迁移是一个关键的早期事件.
- MPA干扰雌激素的保护机制,防止血管损伤.
相关概念视频
Inflammation
Overview
Inflammatory Response I: Vascular and Cellular
The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
Formation of the Platelet Plug
The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
Acute 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...
Acute 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...
Acute 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...


