19.1 Nonspecific Resistance

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19.1Nonspecific Resistance
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Nonspecific Defenses of the Host

• Susceptibility
• Lack of resistance to a disease
• Resistance
• Ability to ward off disease
• Nonspecific resistance
• Defenses against any pathogen
• Specific resistance
• Immunity, resistance to a specific pathogen

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Host Defenses
Figure 16.1
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Mechanical Factors

• Skin
• Epidermis
• consists of tightly packed cells with
• Keratin
• a protective protein

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Mechanical 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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Chemical Factors

• Sebum
• Fungistatic fatty acid
• Low pH
• skin(3-5) gastric juice(1.2-3.0)
• Bile
• Solubilizes lipids
• Lysozyme
• perspiration, tears, saliva, and tissue fluids
• Transferrins
• in blood find iron
• Nitrous Oxide
• 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
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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, some phagocytosis
• Monocytes
• Phagocytic as mature macrophages
• Macrophages
• Fixed in lungs, liver, bronchi
• Wandering roam tissues
• Lymphocytes
• specific immunity

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Phagocytosis

• Phago eat
• Cyte cell
• Ingestion of microbes or particles by a cell
• performed by phagocytes

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Phagocytosis
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Phagocytosis
Figure 16.8a
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Microbial Evasion of Phagocytosis
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Inflammation

• Redness
• Pain
• Heat
• Swelling (edema)
• Acute-phase proteins activated
• complement, cytokine, kinins
• Vasodilation
• histamine, kinins, prostaglandins, leukotrienes
• Margination and emigration of WBCs
• Tissue repair

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Chemicals Released by Damaged Cells
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The Process of Inflammation
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Inflammation
Figure 16.9a, b
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Inflammation
Figure 16.9c, d
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Fever

• Abnormally High Body Temperature
• Hypothalamus normally set at 37C
• Gram-negative endotoxin
• cause phagocytes to release interleukin 1
• Hypothalamus
• releases prostaglandins that reset the
  hypothalamus to a high temperature
• Body increases rate of metabolism and shivering
• to raise temperature
• When IL-1 is eliminated, body temperature falls.
  (Crisis)

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Overview of Complement Function
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The Complement System

• Serum proteins
• activated in a cascade

Figure 16.10
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Effects of Complement Activation

• Opsonization or immune adherence
• enhanced phagocytosis
• Membrane attack complex
• cytolysis
• Attract phagocytes

Figure 16.11
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Effects of Complement Activation
Figure 16.12
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Classical Pathway
Figure 16.13
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Alternative Pathway
Figure 16.14
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Lectin Pathway
Figure 16.15
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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 Beta IFN
• Cause cells to produce antiviral proteins
• inhibit viral replication
• Gamma IFN
• Causes neutrophils and macrophages
• to phagocytize bacteria

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Interferons (IFNs)
New viruses released by the virus-infected host
cell infect neighboring host cells.
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2
The infecting virus replicates into new viruses.
AVPs degrade viral m-RNA and inhibit protein
synthesis and thus interfere with viral
replication.
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Viral RNA from an infecting virus enters the cell.
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The infecting virus also induces the host cell to
produce interferon on RNA (IFN-mRNA), which is
translated into alpha and beta interferons.
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Interferons released by the virus-infected host
cell bind to plasma membrane or nuclear membrane
receptors on uninfected neighboring host cells,
inducing them to synthesize antiviral proteins
(AVPs). These include oligoadenylate synthetase,
and protein kinase.
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Figure 16.16