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Copyright © 2010 Pearson Education, Inc.
INNATE IMMUNITY – NONSPECIFIC DEFENSES OF
THE HOST
CHAPTER 16
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The Concept of Immunity
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
Figure 16.2
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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
Figure 24.7
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Ciliary Escalator
Figure 16.4
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Physical Factors
Lacrimal apparatus: Washes eye Saliva: Washes microbes off Urine: Flows out Vaginal secretions: Flow out
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Lacrimal Apparatus
Figure 16.3
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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
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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Red Blood Cells Transport O2 and CO2
White Blood Cells:
Neutrophils Phagocytosis
Basophiles Histamine
Eosinophils Kill parasites
Formed Elements in Blood
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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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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%
Differential White Cell Count
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Components of Lymphatic System
Figure 16.5a
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The Lymphatic System
Figure 16.5b–c
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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
Figure 16.6
Phagocytic cells: Neutrophils, Fixed macrophages, Wandering macrophages
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Phagocytosis
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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
Acute-phase proteins activated (complement, cytokine, and kinins)
Vasodilation (histamine, kinins, prostaglandins, and leukotrienes)
Redness Swelling (edema) Pain Heat
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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
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
Disadvantages Tachycardia Acidosis Dehydration 44–46°C fatal
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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
Figure 16.9
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Effects of Complement Activation
Opsonization or immune adherence: Enhanced phagocytosis
Membrane attack complex: Cytolysis Attract phagocytes
Figure 16.10
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Inflammation Stimulated by Complement
Figure 16.11
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Classical Pathway of Complement Activation
Figure 16.12
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Alternative Pathway of Complement Activation
Figure 16.13
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Lectin Pathway of Complement Activation
Figure 16.14
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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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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)
Figure 16.15
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Innate Immunity
Transferrins Bind serum iron
Antimicrobial peptides Lyse bacterial cells
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