L50: Acute Inflammation

Question 1

4 cardinal signs of acute inflammation

Answer 1

Redness: hyperaemia
Swelling: oedema
Pain: bradykinin, PGE2
Heat: hyperaemia

Question 2

Causes of acute inflammation

Answer 2

1. Physical: burns
2. Chemical
3. Biological: bacteria, parasites, fungi
4. Hypersensitivity

Question 3

Components in acute inflammation

Answer 3

1. Neutrophil
   - Primary/azurophilic granules: myeloperoxidase
   - Secondary/specific granules: antibacterial protein (lysozyme)
2. Lymphocyte
   - T cell, B cell, NK cell
3. Eosinophil
4. Monocyte / macrophages
5. Platelets
6. Endothelial cells
7. Fibroblast

Question 4

Protein / Chemical Mediators that modulate inflammatory response

Answer 4

Cell-derived / Serum-derived

1. Histamine (mast cell granules)
   - Vasodilation
   - ↑ vascular Permeability
2. Prostaglandins (cell membrane)
3. Leukotriene (cell membrane)
4. Bradykinin + Kallikrein
5. Adhesion molecules
6. TNF-alpha + IL-1 (macrophages)
   - cause production of Prostaglandin (↑ thermal set point —> shivering, vasoconstriction, fever, heat conservation)
   - ↑ Adhesion molecules on endothelium for neutrophil to stick and migrate
   - ↑ Acute phase protein (C-reactive protein)
7. Complement
   - C3a + C5a: anaphylatoxin: vasodilation + ↑ permeability
   - C3a: macrophage activation + mast cell degranulation
   - C5a: mast cell degranulation
   - C5b + C6-C9: MAC
   - C3b: opsonin
8. Antibody
   - IgG

Question 6

Phases of acute inflammation

Answer 6

1. Vascular phase
   - Vasodilator (mast cells, basophils, neutrophils, platelets) —> Hyperaemia

• Open gap junction —> ↑ vascular permeability —> LMW protein move out
• Plasma flows out —> Oedema —> extracellular fluid contains HMW protein / WBC / fibrinogen —> Exudate

2. Cellular phase
   - Leukocyte movement
   —> Rolling: neutrophil rolling along vessel (low adhesion with adhesion molecules on endothelium)
   —> Margination: neutrophil adhere to endothelium via adhesion molecules
   —> Emigration: push through 2 endothelial cells and basement membrane
   —> Chemotaxis: attracted by chemotaxin (e.g. C5a) from bacteria / injured cells

• Opsonisation: antibody + C3b —> promotes attachment of phagocyte
• Phagocytosis: phagosome formation
• Intracellular killing: phagolysosome formation —> myeloperoxidase + other oxygen independent mechanism
• TNF-alpha + IL-1 production: fever
• Antigen presentation: T cell —> stimulate B cell —> plasma cells —> antibody —> specific immune response