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TORTORA  FUNKE  CASE
ninth edition
MICROBIOLOGY
an introduction
16
Innate Immunity:
Nonspecific Defenses
of the Host
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Nonspecific Defenses of the Host
 Susceptibility: Lack of resistance to a disease.
 Immunity: Ability to ward off disease.
 Innate immunity: Defenses against any pathogen.
 Adaptive immunity: Immunity, resistance to a specific
pathogen.
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Host Defenses
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Figure 16.1
First line of defense (Non-specific resistance)
 Physical and Chemical Defenses
 Normal Flora
Second line of defense (Non-specific resistance)
 Phagocytosis
 Inflammation
 Fever
 Antimicrobial substances: Complement, Interferon
Third line of defense (Specific Resistance)
 Antibodies
 B cells and T cells
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Physical Factors
 Skin
 Epidermis consists of tightly packed cells with
 Keratin, a protective protein
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Physical Factors
 Mucous membranes
 Ciliary escalator:
Microbes trapped in mucus
are transported away from
the lungs.
 Lacrimal apparatus:
Washes eye.
 Saliva: Washes microbes off.
 Urine: Flows out.
 Vaginal secretions: Flow out.
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Figure 16.4a
Chemical Factors
 Fungistatic fatty acid in sebum.
 Low pH (3-5) of skin.
 Lysozyme in perspiration, tears, saliva, and tissue
fluids.
 Low pH (1.2-3.0) of gastric juice.
 Transferrins in blood find iron.
 NO inhibits ATP production.
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Normal Microbiota
 Microbial antagonism/competitive exclusion: Normal
microbiota compete with pathogens.
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Formed Elements in Blood
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Table 16.1 (1 of 2)
Formed Elements in Blood
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Table 16.1 (2 of 2)
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%
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White Blood Cells
 Neutrophils: Phagocytic
 Basophils: Produce histamine
 Eosinophils: Toxic to parasites and some phagocytosis
 Dendritic cells: Initiate adaptive immune response
 Monocytes: Phagocytic as mature macrophages
 Fixed macrophages in lungs, liver, and bronchi
 Wandering macrophages roam tissues.
 Lymphocytes: Involved in specific immunity.
PLAY
Animation: Host Defenses
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Toll-like receptors: What are some evolutionarily conserved
features of microbes that our immune cells could recognize?
Step 2.
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cytokines
The largest group of cytokines stimulates immune
cell proliferation and differentiation. This group
includes Interleukin 1 (IL-1), which activates T
cells; IL-2, which stimulates proliferation of
antigen-activated T and B cells; IL-4, IL-5, and IL6, which stimulate proliferation and differentiation
of B cells; Interferon gamma (IFNg), which
activates macrophages; and IL-3, IL-7 and
Granulocyte Monocyte Colony-Stimulating Factor
(GM-CSF), which stimulate hematopoiesis.
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Phagocytosis
 Phago: from Greek,
meaning eat
 Cyte: from Greek,
meaning cell
 Ingestion of microbes
or particles by a cell,
performed by
phagocytes.
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Figure 16.6
Phagocytosis
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Figure 16.7
Microbial Evasion of Phagocytosis
Inhibit adherence: M protein,
capsules
Streptococcus pyogenes, S. pneumoniae
Kill phagocytes: Leukocidins
Staphylococcus aureus
Lyse phagocytes: Membrane
attack complex
Listeriamonocytogenes
Escape phagosome
Shigella
Prevent phagosome-lysosome HIV
fusion
Survive in phagolysosome
PLAY
Coxiella burnetti
Animation: Phagocytosis
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Inflammation
 Redness
 Pain
 Heat
 Swelling (edema)
 Acute-phase proteins activated (complement, cytokine,
and kinins)
 Vasodilation (histamine, kinins, prostaglandins, and
leukotrienes)
 Margination and emigration of WBCs
 Tissue repair
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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
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Inflammation
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Figure 16.8a–b
Inflammation
PLAY
Animation: Inflammation
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Figure 16.8c–d
The movement of phagocytes in the direction of an infection, due to
attraction by complement, chemicals released by microorganisms, and
the remnants of damaged cell membranes is a process called
A) phagocytosis.
B) chemotaxis.
C) diapedesis.
D) cytoadherence.
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Fever: Abnormally High Body Temperature
 Hypothalamus normally set at 37°C.
 Gram-negative endotoxins (so-called pyrogens) cause
phagocytes to release interleukin–1 (IL–1)
 Hypothalamus releases prostaglandins that reset the
hypothalamus to a high temperature.
 Body increases rate of metabolism and shivering which
raise temperature.
 When IL–1 is eliminated, body temperature falls (crisis).
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FEVER
 Hypothalamus controls
body temp
 Pyrogens resets temp set
point
 Pyrogens: cytokines; LPS
 Unfavourable for bacterial
replication
 Favourable for immune
response--phagocytosis;
lymphocyte replication etc
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The Complement System
 Serum proteins
activated in a
cascade.
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Figure 16.9
The Complement System
 Activated in 3 ways
 Antibody-antigen (augments specific defense)
 Molecules that recognize bacterial sugar polymer
(mannan)
 “Random binding” to cell surfaces (C3b)
 Triggers a cascade
 3 effects
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Effects of Complement Activation
 Opsonization or
immune adherence:
Enhanced
phagocytosis.
 Membrane attack
complex: Cytolysis.
 Attract phagocytes.
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Figure 16.10
Effects of complement system
1. Opsonization
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2. Membrane Attack Complex (Lysis)
Are G+ or G-ve cells more susceptible to killing by MAC? Why?
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3. Inflammation
 What else triggers
inflammation? Tissue
damage
 What are features of
inflammation?
 What is the inflammatory
process?
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Effects of Complement Activation
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Figure 16.11
Some Bacteria Evade Complement
 Capsules prevent C activation.
 Surface lipid-carbohydrates prevent MAC formation.
 Enzymatic digestion of C5a.
PLAY
Animation: The Complement System
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Interferons (IFNs)
 Alpha IFN and Beta IFN: Cause cells to produce
antiviral proteins that inhibit viral replication.
 Gamma IFN: Causes neutrophils and macrophages
to phagocytize bacteria.
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Interferon and viral infections: a protective alerting system
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