Download BIOL260 Chapter 16 Lecture

INNATE IMMUNITY –
NONSPECIFIC DEFENSES OF
THE HOST
CHAPTER 16
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The Concept of Immunity
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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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The Concept of Immunity
 Host Toll-like receptors (TLRs) attach to
 Pathogen-associated molecular patterns
(PAMPs)
 TLRs induce cytokines that regulate the intensity
and duration of immune responses
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Physical Factors
 Skin
 Epidermis
consists of tightly
packed cells with
 Keratin, a
protective protein
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Figure 16.2
Physical Factors
 Mucous membranes
 Mucus: Traps microbes
 Ciliary escalator: Microbes trapped in mucus are
transported away from the lungs
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Ciliary Escalator
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Figure 24.7
Ciliary Escalator
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Figure 16.4
Physical Factors
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Lacrimal apparatus: Washes eye
Saliva: Washes microbes off
Urine: Flows out
Vaginal secretions: Flow out
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Lacrimal Apparatus
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Figure 16.3
Q&A
During one year,
nosocomial infections
occurred in 74 patients in
one hospital. All 74
patients were intubated
and mechanically
ventilated. The infections
were caused by
Burkholderia cepacia
transmitted in nonsterile
mouthwash.
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Q&A
Why did these patients
develop infections
while others who used
the mouthwash were
not infected?
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Chemical Factors
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Fungistatic fatty acid in sebum
Low pH (3–5) of skin
Lysozyme in perspiration, tears, saliva, and urine
Low pH (1.2–3.0) of gastric juice
Low pH (3–5) of vaginal secretions
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Normal Microbiota and Innate
Immunity
 Microbial antagonism/competitive exclusion:
Normal microbiota compete with pathogens or
alter the environment
 Commensal microbiota: One organism (microbe)
benefits and the other (host) is unharmed
 May be opportunistic pathogens
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Formed Elements in Blood
Red Blood Cells
Transport O2 and CO2
White Blood Cells:
Neutrophils
Phagocytosis
Basophiles
Histamine
Eosinophils
Kill parasites
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Formed Elements in Blood
Monocytes
Phagocytosis
Dendritic cells
Phagocytosis
Natural killer cells
Destroy target cells
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Formed Elements in Blood
T cells
Cell-mediated immunity
B cells
Produce antibodies
Platelets
Blood clotting
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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%
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Components of Lymphatic System
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Figure 16.5a
The Lymphatic System
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Figure 16.5b–c
Phagocytosis
 Phago: From
Greek, meaning eat
 Cyte: From Greek,
meaning cell
 Ingestion of
microbes
or particles by a
cell, performed by
phagocytes
Phagocytic cells: Neutrophils, Fixed macrophages,
Wandering macrophages
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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
Listeria monocytogenes
Escape phagosome
Shigella, Rickettsia
Prevent phagosome-lysosome HIV, Mycobacterium tuberculosis
fusion
Survive in phagolysosome
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Coxiella burnettii
Inflammation
 Acute-phase proteins activated (complement,
cytokine, and kinins)
 Vasodilation (histamine, kinins, prostaglandins,
and leukotrienes)
 Redness
 Swelling (edema)
 Pain
 Heat
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Chemicals Released by Damaged Cells
Histamine
Vasodilation, increased permeability
of blood vessels
Kinins
Vasodilation, increased permeability
of blood vessels
Intensity histamine and kinin effect
Prostaglandins
Leukotrienes
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Increased permeability of blood vessels,
phagocytic attachment
The Process of Inflammation
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Figure 16.8a, b
Phagocyte Migration and Phagocytosis
[Insert Animation Inflammation: Overview, Steps.]
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Figure 16.8c
Tissue Repair
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Figure 16.8d
Fever
 Abnormally high body temperature
 Hypothalamus normally set at 37°C
 Gram-negative endotoxin 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
 Vasodilation and sweating: Body temperature falls
(crisis)
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Fever
 Advantages
 Increases transferrins
 Increases IL–1 activity
 Produces Interferon
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 Disadvantages
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Tachycardia
Acidosis
Dehydration
44–46°C fatal
The Complement System
 Serum proteins activated in a cascade
 Activated by
 Antigen-antibody reaction
 Proteins C3, B, D, P and a pathogen
 C3b causes opsonization
 C3a + C5a cause inflammation
 C5b + C6 + C7 + C8 + C9 cause cell lysis
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The Complement System
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Figure 16.9
Effects of Complement Activation
 Opsonization or immune adherence: Enhanced
phagocytosis
 Membrane attack complex: Cytolysis
 Attract phagocytes
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Figure 16.10
Inflammation Stimulated by
Complement
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Figure 16.11
Classical Pathway of Complement
Activation
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Figure 16.12
Alternative Pathway of Complement
Activation
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Figure 16.13
Lectin Pathway of Complement
Activation
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Figure 16.14
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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Interferons (IFNs)
 IFN- and IFN-: Cause cells to produce antiviral
proteins that inhibit viral replication
 Gamma IFN: Causes neutrophils and macrophages
to phagocytize bacteria
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Antiviral Actions of Interferons (IFNs)
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Figure 16.15
Innate Immunity
 Transferrins
 Bind serum iron
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 Antimicrobial peptides
 Lyse bacterial cells