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Lecture 2

PAT20A/B Lecture 2: (2)PAT20 Fall Week 2 Notes (Inflammation)


Department
Pathotherapeutics
Course Code
PAT 20A/B
Professor
Audrey Kenmir
Lecture
2

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(2)PAT20 Fall Week 2 Notes (Inflammation)
By: Bina Nsimba
Inflammatory Response
- Inflammatory response: a sequential reaction to cell injury that neutralizes and dilutes the
inflammatory agent, removes necrotic materials, and establishes an environment suitable
for healing and repair.
- Infection: involves invasion of tissues or cells by microorganisms such as bacteria, fungi,
and viruses.
a) Vascular
1. Sympathetic nervous system stimulates arterioles in the area to briefly undergo
transient vasoconstriction.
2. Platelets adhere to vessels and aggregate, forming a fibrin-platelet clot to seal the
injured area, and release proinflammatory mediators (ex. histamine, cytokines,
and prostaglandins) which causes vasodilation.
3. Hyperemia (increased blood flow in the area) causes filtration pressure increases,
which causes endothelial cell retraction and increased capillary permeability.
4. Fluid moves from capillaries into tissue spaces.
5. Inflammatory serous exudate later contains plasma proteins (ex. albumin), which
exerts oncotic pressure that further draws fluid from blood vessels, which causes
edema in tissue.
6. Fibrinogen (plasma protein) leaves the blood, and is activated by the products of
the injured cells to become fibrin (blood clot protein), to trap, kill, and prevent the
spread of bacteria.
b) Cellular
1. Phagocytes produce nitric oxide, which inhibit vascular smooth muscle
contraction and growth, platelet aggregation, and leukocyte adhesion to
endothelium.
2. Cytokines are released by macrophages, which causes endothelial cells to express
cellular adhesion molecules (selectins and integrins).
3. The blood flow through capillaries in the area slows as fluid is lost and viscosity
increases.
4. Neutrophils and monocytes move to the inner surface of the capillaries
(margination), and through the capillary wall (diapedesis) to the site of injury
(chemotaxis).
Chemotaxis: mechanism for ensuring accumulation of neutrophils and
monocytes at the focus of injury.
Neurophils
Neutrophils are the first leukocytes to arrive at the site of
inflammation (usually within 6 to 12 hours).
Monocytes

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Monocytes are the second type of phagocytic cells that migrate
from circulating blood (within 3 to 7 days after the onset of
inflammation).
Mediators of Inflammation
Histamine (stored in granules of basophils, mast cells, platelets) = causes vasodilation
and increased vascular permeability by stimulating contraction of endothelial cells and
creating widened gaps between cells.
Serotonin (stored in platelets, mast cells, enterochromaffin cells of GI tract) = causes
vasodilation and increased vascular permeability by stimulating contraction of
endothelial cells and creating widened gaps between cells; stimulates smooth muscle
contraction.
Kinins (e.g., bradykinin) (produced from precursor factor kininogen as a result of
activation of Hageman factor (XII) of clotting system) = cause contraction of smooth
muscle and dilation of blood vessels; result in stimulation of pain.
Complement components (C3a, C4a, C5a) (anaphylatoxic agents generated from
complement pathway activation) = stimulate histamine release; stimulate chemotaxis.
Fibrinopeptides (produced from activation of the clotting system) = increase vascular
permeability; stimulate chemotaxis for neutrophils and monocytes.
Prostaglandins & Leukotrienes (produced from arachidonic acid) = prostaglandins E1 and
E2 cause vasodilation; leukotriene B4 stimulates chemotaxis.
Cytokines (soluble factors secreted by WBCs and a variety of other cells in the body) =
act as messengers between the cell types.
Complement System
The complement system is a major mediator of the inflammatory response.
Major functions of the complement system are enhanced phagocytosis, increased
vascular permeability, chemotaxis, and cellular lysis.
When the complement system is activated, the components are generated in the
sequential order of C1, C4, C2, C3, C5, C6, C7, C8, and C9.
The numbering reflects the order of their discovery.
The primary pathway for activation of the complement system is through fixation
of component C1 to an antigen-antibody complex.
Immunoglobulins G and M are responsible for fixing complement.
An alternative pathway exists in which C3 is activated without prior antigen-
antibody fixation.
Bacterial products, lipopolysaccharides, and neutrophil proteases can stimulate
the complement sequence at the C3 level with activation of C5 through C9.
Complement activation increases phagocytosis through opsonization and
chemotaxis.
Opsonization: occurs when the antigen, in combination with complement factor
C3b and immunoglobulin, sticks to the surface of phagocytic cells, leading to
more rapid phagocytosis.
Complement component C5a promotes chemotaxis.
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