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急性炎症 II：细胞阶段
急性炎症的细胞阶段是一系列高度协调的事件，其主要将白细胞（尤其是中性粒细胞）募集至组织损伤或感染部位。在初始的血管变化之后，该阶段可确保免疫细胞有效迁移、活化并发挥功能，以清除病原体并启动组织修复。
白细胞募集级联反应
白细胞募集过程分为四个步骤：边集、黏附、转迁移和趋化。血流减慢导致白细胞向血管壁移动…
急性炎症的细胞阶段包括将白细胞募集到损伤部位的步骤。
首先是边集，即随着血流减慢和黏度增加，白细胞向血管壁移动。随后是滚动，此时白细胞与内皮细胞选择素发生松散的结合与解离。
接下来，在牢固黏附阶段，白细胞整合素会紧密地结合到内皮细胞黏附分子（如 ICAM-1 和 VCAM-1）上。
接着，在血细胞渗出过程中，白细胞通过挤压内皮细胞之间的间隙进入组织。
在吞噬溶酶体内，病原体被活性氧和蛋白水解酶降解。
完成其功能后，中性粒细胞会经历凋亡，并通常被巨噬细胞安静地清除。
如果清除延迟，这些酶可能会渗入周围组织，持续引发炎症过程。
如果消除有害刺激，抗炎信号和促消退介质将恢复组织稳态。
持续或未消退的炎症可能转变为慢性炎症。
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Q1: What is margination in the cellular phase of acute inflammation?
Margination is the first step of leukocyte recruitment where reduced blood flow causes leukocytes to move toward the vessel wall as blood viscosity increases. This positioning along the endothelium prepares cells for the subsequent rolling and adhesion phases, enabling their eventual migration into inflamed tissue.
Q2: How do leukocytes move from rolling to firm adhesion?
During rolling, leukocytes loosely bind and unbind to endothelial selectins. Firm adhesion occurs when leukocyte integrins such as LFA-1 and Mac-1 bind tightly to endothelial adhesion molecules like ICAM-1 and VCAM-1. This tight binding halts rolling motion and anchors cells in preparation for tissue entry through diapedesis.
Q3: What happens during diapedesis in acute inflammation?
Diapedesis is the process where leukocytes squeeze between endothelial cells to enter tissue. Molecules such as PECAM-1 facilitate this transmigration. Once in the interstitial space, leukocytes respond to chemoattractants including IL-8, C5a, and leukotriene B4, which guide them to the precise injury site.
Q4: How do neutrophils destroy pathogens inside phagolysosomes?
Neutrophils engulf pathogens into phagosomes that fuse with lysosomes to form phagolysosomes. Inside, reactive oxygen species and proteolytic enzymes break down and destroy the pathogens. After completing their antimicrobial role, neutrophils undergo apoptosis and autophagy, then are normally cleared quietly by macrophages.
Q5: What causes tissue damage when neutrophil clearance is delayed?
If macrophage clearance of apoptotic neutrophils is delayed, neutrophil enzymes may leak into surrounding tissue and continue the inflammatory process, causing additional damage. This enzyme release extends inflammation beyond its intended protective role and can worsen tissue injury at the inflammation site.
Q6: How does acute inflammation resolve when the injury is eliminated?
When the injurious stimulus is eliminated, anti-inflammatory signals and pro-resolving mediators restore tissue homeostasis, allowing inflammation to resolve. If the cause persists or inflammation remains unresolved, it may transition into chronic inflammation, requiring different immune mechanisms for resolution and management.
Q7: What is the role of chemotaxis in leukocyte recruitment?
Chemotaxis is the directed migration of leukocytes in response to chemoattractants released at injury sites. Key chemotactic agents include interleukin-8, complement component C5a, and leukotriene B4. These chemical signals guide neutrophils and other leukocytes precisely to the location of tissue damage or infection.