The Extravasation (Diapedesis) of Leukocytes


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A diagram with 3 steps. The first step states: leukocytes in the blood respond to chemical attractants released by pathogens and chemical signals from nearby injured cells. An injury to the surface of the skin is labeled: injured/infected cells secrete chemical signals into the blood. Pathogens are present in the wound. Neutrophils and monocytes are in the blood stream; and the outside of the vessel is labeled capillary epithelial cells. A resident macrophage engulfs the pathogens and releases proinflammatory chemotactic cytokines. The second step states: the leukocytes squeeze between the cells of the capillary wall as they follow the chemical signals to where they are most concentrated (positive chemotaxis). The leukocytes emigrate to the site of injury and infection. The chemical signals present include C5a and cytokines. The third panel states: Within the damaged tissue, neutrophils release chemicals that break apart pathogens. Monocytes differentiate into macrophages. Neutrophils and macrophages phagocytize pathogens and cellular debris. Neutrophils release cytotoxic chemicals from granules into tissue.
Damaged cells and macrophages that have ingested pathogens release cytokines that are proinflammatory and chemotactic for leukocytes. In addition, activation of complement at the site of infection results in production of the chemotactic and proinflammatory C5a. Leukocytes exit the blood vessel and follow the chemoattractant signal of cytokines and C5a to the site of infection. Granulocytes such as neutrophils release chemicals that destroy pathogens. They are also capable of phagocytosis and intracellular killing of bacterial pathogens.

Source: OpenStax Microbiology

OpenStax Microbiology

Some phagocytes are leukocytes (WBCs) that normally circulate in the bloodstream. To reach pathogens located in infected tissue, leukocytes must pass through the walls of small capillary blood vessels within tissues. This process, called extravasation, or diapedesis, is initiated by complement factor C5a, as well as cytokines released into the immediate vicinity by resident macrophages and tissue cells responding to the presence of the infectious agent. Similar to C5a, many of these cytokines are proinflammatory and chemotactic, and they bind to cells of small capillary blood vessels, initiating a response in the endothelial cells lining the inside of the blood vessel walls. This response involves the upregulation and expression of various cellular adhesion molecules and receptors. Leukocytes passing through will stick slightly to the adhesion molecules, slowing down and rolling along the blood vessel walls near the infected area. When they reach a cellular junction, they will bind to even more of these adhesion molecules, flattening out and squeezing through the cellular junction in a process known as transendothelial migration. This mechanism of “rolling adhesion” allows leukocytes to exit the bloodstream and enter the infected areas, where they can begin phagocytosing the invading pathogens.

Note that extravasation does not occur in arteries or veins. These blood vessels are surrounded by thicker, multilayer protective walls, in contrast to the thin single-cell-layer walls of capillaries. Furthermore, the blood flow in arteries is too turbulent to allow for rolling adhesion. Also, some leukocytes tend to respond to an infection more quickly than others. The first to arrive typically are neutrophils, often within hours of a bacterial infection. By contract, monocytes may take several days to leave the bloodstream and differentiate into macrophages.


Parker, N., Schneegurt, M., Thi Tu, A.-H., Forster, B. M., & Lister, P. (n.d.). Microbiology. Houston, Texas: OpenStax. Access for free at: