Innate Immunity: Nonspecific Defenses of the Host

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Chapter 16

• Innate Immunity Nonspecific Defenses of the Host

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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
Figure 16.1
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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.

Figure 16.4a
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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
Table 16.1 (1 of 2)
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Formed Elements in Blood
Table 16.1 (2 of 2)
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Differential White Cell Count

• Percentage of each type of white cell in a sample
  of 100 white blood cells.

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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.

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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
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Phagocytosis
Figure 16.7
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Microbial Evasion of 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
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Inflammation
Figure 16.8ab
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Inflammation
Figure 16.8cd
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Fever Abnormally High Body Temperature

• Hypothalamus normally set at 37C.
• Gram-negative endotoxin cause phagocytes to
  release interleukin1 (IL1).
• Hypothalamus releases prostaglandins that reset
  the hypothalamus to a high temperature.
• Body increases rate of metabolism and shivering
  which raise temperature.
• When IL1 is eliminated, body temperature falls
  (crisis).

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Fever

• Advantages
• Increase transferrins
• Increase IL1 activity

• Disadvantages
• Tachycardia
• Acidosis
• Dehydration

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The Complement System

• Serum proteins activated in a cascade.

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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Effects of Complement Activation
Figure 16.11
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Classical Pathway
Figure 16.12
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Alternative Pathway
Figure 16.13
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Lectin Pathway
Figure 16.14
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Some Bacteria Evade Complement

• Capsules prevent C activation.
• Surface lipid-carbohydrates prevent MAC
  formation.
• Enzymatic digestion of C5a.

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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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Interferons (IFNs)
Figure 16.15
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Innate Immunity

• Transferrins
• Bind serum iron

• Antimicrobial peptides
• Lyse bacterial cells