Innate Immunity: Nonspecific

Defenses of the Host

Chapter 16
 IM MUNIT Y

1. Innate Immunity

2. A daptive Immunity
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Figure 16.1
 F irst-line Defenses
1. Physical Bar riers
Skin, M ucous M embrane
2. A ntimicrobial Substances
L ysozyme: tears, saliva
L actofer rins and T ransfer rins
Defensins
Peroxidase
 F irst-line Defenses

3. Normal F lora
Competitive E xclusion
Production of toxins
A lteration of E nvironment
C ells of the Immune System
H ematopoietic Stem cell

Blood cells:
R B Cs
platelets
W B Cs
 W B Cs/L eukocytes
1. G ranulocytes
Neutrophils
Eosinophils
Basophils
2. Mononuclear phagocytes
M acrophages
Dendritic cells
 Formed Elements in Blood

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 Formed Elements in Blood

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 W B Cs/L eukocytes
3. L ymphocytes
T and B lymphocytes

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 Formed Elements in Blood

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 Differential White Cell Count
‡ Percentage of each type of white cell in a sample
of 100 white blood cells

Neutrophils 60±70%
Basophils 0.5±1%

Eosinophils 2±4%

Monocytes 3±8%

Lymphocytes 20±25%
 Phagocytosis
Process of Phagocytosis:
1. C hemotaxis
2. Recognition and attachment
3. E ngulfment: phagosome
4. Formation of a phagolysosome
5. Digestion
6. E xocytosis
Phagocytosis

Figure 16.7
 The Concept of Immunity
‡ Host Toll-like receptors (T L Rs) attach to
‡ Pathogen-associated molecular patterns
(P A M Ps)
‡ TLRs induce cytokines that regulate the intensity
and duration of immune responses
 Microbial Evasion of Phagocytosis

Inhibit adherence: M protein, Streptococcus pyogenes, S. pneumoniae

capsules
Kill phagocytes: Leukocidins Staphylococcus aureus

Lyse phagocytes: Membrane Listeria monocytogenes

attack complex
Escape phagosome Shigella, Rickettsia

Prevent phagosome-lysosome HIV, Mycobacterium tuberculosis

fusion
Survive in phagolysosome Coxiella burnettii
 Inflammation
1. Local Response
2. Symptoms :
Redness: Rubor
H eat: C alor
Pain: Dolor
Swelling: E dema
 Inflammation
3. C auses:

4. F unction:
Destroy injurious agent
L imit the spread
Repair damaged tissue
 Process of Inflammation
1. T rigger
2. V asodilation and increased
permeability of blood vessels
3. Phagocyte migration (Diapedesis)and
phagocytosis(P M N vs. macrophages)
4. T issue Repair
Pus formation
 Chemicals Released by Damaged
Cells

Histamine Vasodilation, increased permeability

of blood vessels
Kinins Vasodilation, increased permeability
of blood vessels
Prostaglandins Intensity histamine and kinin effect
Leukotrienes Increased permeability of blood vessels,
phagocytic attachment
The Process of Inflammation

Figure 16.8a, b
Phagocyte Migration and Phagocytosis

[Insert Animation Inflammation: Overview, Steps.]

Figure 16.8c
Tissue Repair

Figure 16.8d
 F ever
1. systemic response to an infection

2. W hat causes?
M acrophages-I L1Æhypothalamus

3. How is host helped?

 I N T E R F E R O NS
1. W ho produces?

2. W hat are they and how do they act?

 Interferons (IFNs)
‡ I F N-D and I F N-E: C ause cells to produce
antiviral proteins that inhibit viral replication

‡ G amma I F N: C auses neutrophils and

macrophages to phagocytize bacteria
Antiviral Actions of Interferons
(IFNs)

Figure 16.15
 T he Complement System
1. W hat is it?

2. A ctivated in three different ways

-C lassical Pathway
-L ectin Pathway
-A lternative Pathway
Classical Pathway of Complement Activation

Figure 16.12
 Consequences of complement
activation
1. O psonization: C3b is an opsonin

2. Inflammation: C3a and C5a

3. C ytolysis: M embrane A ttack Complex

The Complement System

Figure 16.9
 The Complement System
‡ C3b causes opsonization
‡ C3a + C5a cause inflammation
‡ C5b + C6 + C7 + C8 + C9 cause cell lysis
Inflammation Stimulated by
Complement

Figure 16.11
 Some Bacteria Evade Complement
‡ Capsules prevent C activation
‡ Surface lipid-carbohydrates prevent membrane
attack complex (MAC) formation
‡ Enzymatic digestion of C5a