Inflammation Process
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.
Enables 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. Prevents blood loss and provides a
barrier to microorganisms;
Fibrous connective tissue is brought in to repair
the damage
When healing is complete the blood clot is
removed