Lecture # 25
ACUTE INFLAMMATION-2
Dr. Iram Sohail
Assistant Professor
Pathology
College Of Medicine
Majmaah University
OBJECTIVES
• Discuss the mechanism of acute inflammation
• Enlist the features of acute inflammation
MECHANISM OF ACUTE INFLAMMATION
• Acute inflammation is a rapid response to
injury, microbes or foreign body that is
designed to deliver leukocytes and plasma
proteins to the site of injury for the clearance
of microbes and getting rid of necrotic tissue.
Acute inflammation has 2 main components
1. Vascular changes
– Vasodilation
– Increased vascular permeability
2. Cellular events
1. Vascular changes
A. Changes in vascular caliber
i.
Transient vasoconstriction
ii. Vasodilation
– Resulting in increased blood flow to the site of
injury for delivering more fluid and leukocytes.
This is the cause of warmth and redness which we
noticed at the site of acute inflammation.
B. Increased vascular permeability
To deliver the WBCs & fluid at the site of injury
This fluid will be transudate or exudate.
Transudate
• Ultra filtrate of plasma composed of more
fluid and less protein.
Exudate
• Protein & cells rich fluid
• Several mechanisms may contribute to
increased vascular permeability
– Endothelial cell contraction
– Endothelial injury
– Leakage from new blood vessels
(Fluid leakage results in edema)
2. Cellular events
• An important function of inflammatory
response to deliver leukocytes at the site of
injury and then these leukocytes will kill
bacteria and eliminate necrotic tissue.
Cellular events
– Emigration of WBCs from circulation to the site of
injury.
• The principle leukocyte (WBC) in acute
inflammation
is neutrophil.
i. Leukocyte recruitment
Margination
– Leukocyte accumulation at periphery of vessels
Rolling
– Leukocytes roll & stick to endothelial cells
Adhesion to endothelium
– With the help of following adhesion molecules
Endothelial Molecule
Leukocyte Molecule
Major Role
P-selectin
Sialyl-Lewis X-modified proteins
Rolling (neutrophils, monocytes,
lymphocytes)
E-selectin
Sialyl-Lewis X-modified proteins
Rolling and adhesion (neutrophils,
monocytes, T lymphocytes)
GlyCam-1, CD34
L-selectin
Rolling (neutrophils, monocytes)*
ICAM-1 (immunoglobulin family)
CD11/CD18 integrins (LFA-1, Mac-1)
Adhesion, arrest, transmigration
(neutrophils, monocytes, lymphocytes)
VCAM-1 (immunoglobulin family)
VLA-4 integrin
Adhesion (eosinophils, monocytes,
lymphocytes)
CD31
CD31
Transmigration (all leukocytes)
Transmigration between endothelial cells
– Transmigration of leukocytes by squeezing
between cells at intercellular junctions
(diapedesis)
Chemotaxis
– Leukocytes migrate towards site of injury or
infection with the help of chemotactic agents
(cytokines, chemokines, complements)
ii. Leukocyte activation
– These leukocytes first activated by different
stimuli.
– Then killing of bacteria/particle occurs by the
process of phagocytosis.
Phagocytosis
• It is a process by which leukocytes engulf &
destroy bacteria/particle.
• 3 steps
I. Recognition and attachment of particle with
leukocyte (opsonization)
II. Engulfment of particle
• Pseudopods extend around the object and
form a phagocytic vacuole; this will fuse with
lysosome and forms a phagolysosome
III. Killing & degradation of ingested material
• Lysosomal enzymes & reactive oxygen species
(super oxide, hydrogen peroxide) will kill the
microbe.
FEATURES OF ACUTE INFLAMMATION
There are 5 cardinal signs/ features of acute
inflammation.
1. Calor (Heat)
2. Rubor (redness)
3. Tumor (swelling)
4. Dolor (pain)
5. Functio laesa (loss of function)
End results (outcome) of Acute Inflammation
1. Resolution
• complete return to normal of tissue if injury is
eliminated
2. Tissue destruction and persistent of
inflammation
3. Progression to chronic inflammation
4. Healing by fibrosis (scar formation)