Mechanism of Inflammation

• Mechanism of Inflammation is a multi-step process involving changes in vascular permeability, blood flow, and the migration of white blood cells (WBCs) to the site of injury or infection.
• Mechanism of Inflammation to Understanding these mechanisms is crucial for developing treatments that can modulate the inflammatory response.

Key Mechanisms

1. Alteration in Vascular Permeability and Blood Flow

1. Vasodilation

   • Immediate Response: After injury, local blood vessels dilate due to the release of chemical mediators like histamine and nitric oxide.
   • Effects: Increased blood flow causes redness and heat in the affected area.

2. Increased Vascular Permeability

   • Endothelial Cell Contraction: The cells lining the blood vessels contract, creating gaps that allow plasma proteins and leukocytes to exit the bloodstream.
   • Result: Accumulation of fluid in tissues leads to swelling (edema).

3. Exudation

   • Fluid Movement: The movement of fluid and plasma proteins into the tissue is called exudation.
   • Composition: Contains immune cells, nutrients, and antibodies essential for fighting infection and repairing tissue.

2. Migration of White Blood Cells (WBCs)

1. Margination

   • Peripheral Movement: Slowed blood flow causes WBCs, especially neutrophils, to move to the vessel walls (marginate).

2. Rolling and Adhesion

   • Interaction with Endothelium: WBCs roll along and adhere to the endothelial surface via adhesion molecules (e.g., integrins on WBCs and selectins on endothelial cells).
   • Enhancement by Mediators: Cytokines and other mediators enhance this adhesion process.

3. Transmigration (Diapedesis)

   • Crossing the Vessel Wall: WBCs extend pseudopods between endothelial cells, squeezing through gaps to enter surrounding tissue.

4. Chemotaxis

   • Directed Movement: WBCs migrate toward the injury site, guided by chemical signals like chemokines and components of the complement system.

5. Phagocytosis

   • Engulfing Pathogens: Neutrophils and macrophages engulf and digest pathogens, debris, and dead cells.
   • Recognition: Targets are recognized 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.

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