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Why do white blood cells move toward blood-vessel walls during inflammation?

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Pathways of complement activation — inflammation The main function of complement proteins is to aid in the destruction of pathogens by piercing their outer membranes (cell lysis) or by making them more attractive to phagocytic cells such as macrophages (a process known as opsonization). Some complement components also promote inflammation by stimulating cells to release histamine and by attracting phagocytic cells to the site of infection.

During the inflammatory response, blood vessels undergo vasodilation, which increases blood flow to the injured area. Subsequently, the vessel walls become more permeable, allowing protein-rich fluid to exit into the surrounding tissues. As this fluid and other substances leak out, the blood flow within the vessel becomes more sluggish.1

This reduction in flow velocity causes white blood cells to fall out of the central axial stream and move toward the vessel walls. Once they reach the periphery, these cells adhere to the vessel wall, which is the essential first step in their emigration into the extravascular space to reach the site of injury. Once outside the vessel, these cells are guided toward the damage by chemotaxis, a process where they follow a concentration gradient of chemical substances released from the injured tissue.12