The Innate Immune Response-Sp10

8/8/2019 The Innate Immune Response-Sp10

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Innate Immunity: NonspecificDefenses of the Host

Chapter 16


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I M M U N I T Y

1. Innate Immunity

2. Adaptive Immunity


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Figure 16.1


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F irst-line Defenses

1. Physical Bar riers

Skin, Mucous Membrane

2. Antimicrobial Substances

Lysozyme: tears,saliva

Lac

tofe

rr ins

and Trans

fe

rr ins

Defensins

Peroxidase


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F irst-line Defenses

3. Normal F lora

Competitive Exclusion

Production of toxins

Alte

ration of Environme

nt


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Cells of the Immune System

Hematopoietic Stem cell

Blood cells:

RB Cs

plate

le

ts

W B Cs


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W B Cs/Leukocytes

1. Granulocytes

Neutrophils

Eosinophils

Basophils

2.

Mononuc

le

ar phagoc

ytes

Macrophages

Dendriticcells


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Formed Elements in Blood

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W B Cs/Leukocytes

3. Lymphocytes

T and B lymphocytes

Professional Phagocytes???


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Formed Elements in Blood

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8)6/33% 4"',06/)#$(2A',2/%

/&0-"&"-) 83'',)63'((2$5


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Percentage of each type of white cell in a sampleof 100 white blood cells

Neutrophils 6070%

Basophils 0.51%

Eosinophils 24%

Monocytes 38%

Lymphocytes 2025%

Differential White Cell Count


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Phagocytosis

Process of Phagocytosis:

1. Chemotaxis

2. Recognition and attachment

3. Engulfment: phagosome

4.

Formation of a phagolys

os

ome

5. Digestion

6. Exocytosis


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Figure 16.7

Phagocytosis


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The Concept of Immunity

Host Toll-like receptors ( T L Rs) attach to Pathogen-associated molecular patterns

(P A MPs)

TLRs induce cytokinesthat regulate the intensityand duration of immune responses


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Inhibit adherence: M protein,

capsules

Streptococcus pyogenes, S. pneumoniae

Kill phagocytes: Leukocidins Staphylococcus aureus

Lyse phagocytes: Membrane

attack complex

Listeria monocytogenes

Escape phagosome Shigella, Rickettsia

Prevent phagosome-lysosome

fusion

HIV, Mycobacterium tuberculosis

Survive in phagolysosome Coxiella burnettii

Microbial Evasion of Phagocytosis


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Inflammation

1. Local Response

2. Symptoms :

Redness: Rubor

Heat: Calor

Pain: DolorSwelling: Edema


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Inflammation

3. Causes:

4. Function:

Destroy injurious agent

L imit the

s

pre

adRepair damaged tissue


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Process of Inflammation

1. Trigger

2. Vasodilation and increasedpermeability of blood vessels

3. Phagocyte migration (Diapedesis)andphagocytosis(PM N vs. macrophages)

4. Tissue Repair

Pus formation


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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

Chemicals Released by Damaged

Cells


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The Process of Inflammation

Figure 16.8a, b


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Phagocyte Migration and Phagocytosis

Figure 16.8c

[Insert Animation Inflammation: Overview, Steps.]


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Tissue Repair

Figure 16.8d


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Fever

1. systemic response to an infection

2. What causes?

Macrophages-I L1 hypothalamus

3. How is host helped?


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I N T E R F E R O N S

1. Who produces?

2. What are they and how do they act?


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Interferons (IFNs)

I F N- and I F N- : Causecells to produceantivir al proteins that inhibit viral replication

Gamma I F N: Causes neutrophils andmacrophages to phagocytize bacter ia

nt v ra ct ons o nter erons


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nt v ra ct ons o nter erons(IFNs)

Figure 16.15


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The Complement System

1. What is it?

2. Activated in three different ways

-Classical Pathway

-Lectin Pathway

-Alternative Pathway

l i l h f l i i


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Classical Pathway of Complement Activation

Figure 16.12


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Consequences of complement

activation1. Opsonization: C3b is an opsonin

2. Inflammation: C3a and C5a

3. Cytolysis: Membrane Attack Complex


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Figure 16.9


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C3b causes opsonization C3a + C5a cause inflammation

C5b + C6 + C7 + C8 + C9 cause cell lysis

I fl ti Sti l t d b


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Inflammation Stimulated by

Complement

Figure 16.11


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Some Bacteria Evade Complement

Capsules prevent C activation Surface lipid-carbohydrates prevent membrane

attack complex (MAC) formation

Enzymatic digestion of C5a

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The Innate Immune Response-Sp10