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GSE Inflammation Process

Inflammation Process–Can't Live with it, Can't live without it!

Mechanism of the Acute Inflammatory Phase

ATTACk plan

"Bring in the troops" -blood flow increases and blood vessels change to allow infection fighting blood cells and large molecules to move from the blood stream into tissue that needs healing.

Destroy invaders / Remove damaged tissue - cells and molecules kill bacteria and remove damaged tissue by inducing the formation of reactive oxygen species (ROS). The cellular and molecular response signals for biochemical changes that cause unwanted cells to destruct.

 

Acute phase protein (APP) molecules orchestrate the responsive action

 

APPs released in response to alarm-signaling cytokines (particularly IL-6) - by most cells (in particular in the arteries, by various immune system cells, E.g. T-cells, macrophages, platelets, and ECs) during infection or injury;

–   Acute Phase Reactants (APRs, a type of APP) are produced (mostly in the liver) and released into the plasma to modulate:

 

✔ Blood clotting;

✔ Vessel dilation/ contraction

✔ Fibrosis (repair fiber/scarring);

✔ Cell proliferation;

✔ Immune cell action;

✔ Cholesterol deposit/removal;

✔ And More.

–   APRs (inflammation triggers) include:

✔ C-reactive Protein (CRP) - a plasma protein that is a benchmark for determining that inflammation is present; CRP in blood plasma can increase 1000-fold with inflammation;

✔ Serum amyloid (SAA)

✔ Fibrinogen

✔ Alpha 1-acid glycoprotein

Acute Inflammation Response

Leukocytes peak /Monocytes transform into phagocytes - monocytes can move quickly (approx. 8-12 hours) to sites of infection in the tissues and divide/differentiate into macrophages and dendritic cells to elicit an immune response. Half of them are stored in the spleen;

Mast cells peak and degranulate - This response initiates the migration of more macrophage cells and fibroblasts to the target stimulated by chemotactic signals from pre-existing fibroblasts, leukocytes and macrophages.

Vessels dilate for 15 minutes to several hours and become more permeable – enabling WBCs and fluids to leave the vessels (manifests as swelling);

Phagocytic WBCs adhere to vessel wall –cytokines increase number of EC adhesion molecules, which then adhere phagocytic WBCs (usually neutrophils) to the vessel wall, which engulf and destroy microbes and debris particles. (In viral infection, lymphocytes rather than neutrophils usually predominate. In certain parasitic infections, eosinophils predominate);

Injurious agents are destroyed or walled off and debris is cleared – by activated specialized blood and connective tissue cells, so that tissue repair can take place;

Blood clot is formed- t- to prevent blood loss and provide a barrier to microorganisms;

Fibrous connective tissue is brought in to repair the damage

When healing is complete the blood clot is removed

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