Nonspecific Host Defenses

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Non-specific Host Defenses

• Chapter 16

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Response to Microbes

• Susceptibility - likely to get disease
• Resistance - unlikely to get disease
• non-specific defense - same response to all
  infections
• specific response - immune response to single
  pathogen

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Host Defenses
Figure 16.1
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Skin

• Skin structure
• top layer is tightly packed dead cells with
  keratin
• underlying epidermis is layers of sheets of cells
• inner dermis is connective tissue
• Protective features
• dry, tight outer layer
• shedding
• layers of cells
• normal flora

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Mucous Membranes

• Layers of cells-that line openings to body
• Goblet cells produce mucus
• prevents drying, traps microbes
• eyes - lacrimal apparatus
• mouth - saliva
• respiratory - cililary escalator
• urogenital - flow of urine and vaginal secretions

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Chemical Factors

• Sebum
• products of normal microbiota
• perspiration
• lysozyme
• gastric juice (acid)
• transferrins

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Normal Microbiota

• Microbes normally present in/on body
• toxic products
• prevent overgrowth of any species
• prevent colonization of pathogens

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Blood Cells

• Erythrocytes
• Granulocytes
• neutrophils - polymorphonuclear
• basophiles
• eosinophiles
• Agranulocytes
• monocytes - macrophages
• lymphocytes - specific immunity

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Phagocytosis

• Ingestion of microbe (particle) by cell
• Cells - neutrophils, macrophages (fixed and
  wandering)
• Process
• chemotaxis - movement toward damage
• adherence to particle
• ingestion - cell projections moves around object
• forms phagosome
• digestion - fusion with lysosome to form
  phagolysosome
• enzymes and toxic products

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Microbial Evasion of Phagocytosis
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Inflammation

• Triggered by damage to cells
• acute or chronic
• Functions
• destroy agent
• limit effects of agent
• repair damage

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Inflammation Process

• Vasodilation -
• caused by release of histamine and other
  chemicals
• increased blood flow and leakage of fluid into
  area
• redness and swelling result
• fibrin clotting around damage
• formation of pus - white blood cells, bacteria,
  dead cells

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Inflammation Process

• Influx of phagocytes -
• neutrophils and macrophages recruited
• diapedesis
• phagocytosis of damaged cells and bacteria
• tissue repair
• regeneration of dermal cells
• possible scar formation

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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
• body temperature controlled by hypothalamus
• pathogen releases LPS that stimulates WBC to
  release interleukins
• interleukin reacts with hypothalamus
• prostaglandins released
• hypothalmus sets temperature higher
• may also be caused by alpha TNF from macrophages
  and mast cells

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Complement

• System of sequentially acting proteins (gt30)
• Each protein in turn activates the next in the
  sequence
• some are split into active fragments
• some bind to mast cells and cause release of
  histamine
• final result in membrane attack complex
• inserts into membrane of cell being attacked
• causes lysis

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The Complement System

• Serum proteins activated in a cascade.

Figure 16.10
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Activation of Complement

• Classical pathway is initiate by antigen-antibody
  reactions
• Alternate pathway is activated by several blood
  proteins (including properdin) and pathogens
• Lectin pathway is stimulated by lectins from
  liver that react with bacteria
• Inherited deficiencies of complement proteins may
  result in recurrent infections

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Interferons

• Host cell specific, not virus specific
• 3 types - a, b, g
• Some produced by cells infected by viruses
• diffuse to neighboring cells
• cause new cells to produce antiviral proteins
• AVP disrupt viral cycle preventing replication of
  virus
• Others stimulate neutrophils and macrophages
• kill bacteria

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Interferons (IFNs)
New viruses released by the virus-infected host
cell infect neighboring host cells.
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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