Immunity System

Faculty of applied science

Department of medical lab
MLS3C/A
 PHOGOCYTOSIS
Phagocytosis is the process by which phagocytic cells engulf
and digest other cells or particles.

Phagocytic cells are early body defense against invading

microorganism, they recognize and digest extracellular
microbial by the process of phagocytosis.
 Pathogen Recognition

Phagocytic cells use two basic molecular mechanism

for the recognition of microorganism:-
Opsonic dependent recognition
Opsonic independent recognition
Opsonic vs opsonic independent phagocytosis
Opsonic phagocytosis mediated by deposition of proteins on
microbes that target them for recognition by specific
phagocytic receptors on leukocytes.

Opsonic independent phagocytosis is mediated by cell

surface receptors on leukocytes that recognize repeating
component common to many different pathogens.
Opsonic Dependent Recognition
 Opsonic Independent Recognition
1. Lectin phagocytosis: is based on binding of microbial
lectin( carbohydrate-carbohydrate linkage).
2. Protein-protein interaction between the peptide sequences
arginine-glycin-aspartic acid(RGD) on the cell surface of
microorganism and RGD receptors found on all phagocytes.
3. Hydrophilic interaction between bacteria and phagocytic
cells.
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4. The recognition of microbial antigen by detecting

conserved molecule structures called pathogen associated
molecules (PAMPs).
These molecules are unique and invariant to microorganism of a
given class. For example lipopolysaccharides of a gram bacteria
and peptidoglycan of gram + bacteria
These and other PAMPs are recognized by receptors on
phagocytic cell surfaces called pattern recognition receptors
(PRRs).
 Inflammation

Inflammation is the biological response of our body to

harmful stimuli of pathogen or injury.
Its a non specific body defense.
The effect of inflammation can be both local and systemic.
 Cardinal signs of Inflammation
Redness
Pain
Odor
altered function
Swelling
 Inflammation

Acute Chronic
 Acute inflammation
1. Begins when injured tissue cells release chemical signals
that activate the inner lining of nearby capillaries.
2. Within the capillaries, selectin( adhesion molecule) are
displayed on the activated endothelial cells.
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3. These molecules attract and attach neutrophils in the blood

stream to the endothelium cells where they encounter the
inflammatory chemicals that acts as activating signals.
4. These signals activate integrins ( adhesion molecules) on
the neutrophils to stick to the endothelium.
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5. The integrins then attached tightly to selectin causing

neutrophils to stick to endothelium and stop rolling.
6. The neutrophils now undergo dramatic shape changes,
squeezing through the endothelium wall into the interstial
tissue, migrating to the site of injury and attack the
pathogens.
7. neutrophils and other leukocytes are attracted to the
infection site by chemotaxins.
 Chronic inflammation

Is a slow process characterized by the formation of new

connective tissue and it usually causes permanent tissue damage.
The persistence of bacteria can stimulate chronic inflammation.
It lasts at least two weeks.
The bacteria that has cell wall, very highly lipid and wax contents
are relatively resistant to phagocytosis and intercellular killing.
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These bacteria and some other microbial pathogens can

survive within macrophages.
In addition, some bacteria produce toxins that stimulate tissue
damaging reactions even after the bacteria death.
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Chronic inflammation is characterized by a dense infiltration

of lymphocytes and macrophages.

If macrophages are unable to destroy the microorganism

during inflammation, the body attempts to wall off and isolate
the site by forming a granuloma.
 Difference between acute and chronic
Features Acute Chronic
Onset Rapid (hours, minutes) Slow ( days)
Cellular infiltration Neutrophils Macrophages,
monocytes, leucocytes
Tissue injury Mild Severe
Local symptoms Prominent Less prominent
 Question
1. What major events occur during an inflammatory reactions
and how do they contribute to pathogen destruction.?
2. How does chronic inflammation differ from acute
inflammation?