Mechanism of Inflammation is a multi-step process involving alterations in vascular permeability, blood flow, and the migration of white blood cells (WBCs) to the site of injury or infection.
Here’s a brief explanation of these key mechanisms:
1. Alteration in Vascular Permeability and Blood Flow (Mechanism of Inflammation)
Vasodilation:
Immediately after injury, local blood vessels dilate due to the release of chemical mediators such as histamine and nitric oxide.
This increases blood flow to the affected area, causing redness and heat.
Increased Vascular Permeability:
The endothelial cells lining the blood vessels contract and create gaps, allowing plasma proteins and leukocytes to exit the bloodstream and enter the tissue.
This leads to the accumulation of fluid, resulting in swelling (edema).
Exudation:
The movement of fluid and plasma proteins into the tissue is called exudation.
This fluid contains immune cells, nutrients, and antibodies essential for fighting infection and repairing tissue.
2. Migration of White Blood Cells (WBCs)
Margination:
As blood flow slows down in the dilated vessels, WBCs, particularly neutrophils, move to the periphery of the blood vessels (marginate).
Rolling and Adhesion:
WBCs roll along the endothelial surface and adhere to it through interactions between adhesion molecules on WBCs (e.g., integrins) and endothelial cells (e.g., selectins and ICAM-1). Chemical mediators like cytokines enhance this process.
Transmigration (Diapedesis):
WBCs extend pseudopods between endothelial cells, squeezing through the gaps created by increased permeability.
They then pass through the basement membrane to enter the surrounding tissue.
Chemotaxis:
Once in the tissue, WBCs move toward the site of injury or infection, guided by chemical signals such as chemokines, bacterial products, and components of the complement system.
Phagocytosis:
Neutrophils and macrophages engulf and digest pathogens, debris, and dead cells.
They recognize these targets through receptors that bind to opsonins (e.g., antibodies, complement proteins) coating the pathogens.
Understanding these mechanisms is crucial for developing treatments that can modulate the inflammatory response, either by enhancing it to fight infections or by reducing it to prevent excessive tissue damage