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INNATE HOST DEFENSES

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					INNATE HOST DEFENSES
      CHAPTER 16




                   1
Host Defenses

       Adaptive
        – Respond after stimulation by the pathogen or
          agent (specific defenses, immune response)


       Innate
        – Prior stimulation not needed (non-specific)
        – Often needed to trigger adaptive defenses



                                                         2
Defense Barriers
       Physical                    Inflammation
        – Skin, mucus membrane       – Response to tissue
          thickness                    damage

       Chemical                    Fever
        – Skin, mucus membrane       – Interleukin-1 (pyrogen)
          factors, enzymes           – Inc. temp too high for
                                       pathogens
       Cellular defenses            – Speeds tissue repair
        – Blood cells                – Increases
                                       interferon/transferrin
                                       production
                                    Molecular defenses
                                     – Interferon
                                     – Complement

                                                                 3
Physical Barriers

       Skin
        – Stratified
        – Close intercellular junctions
        – Waterproof, dead cells
       Mucous membranes
        – Simple epithelium
        – Mucus layer



                                          4
Chemical Barriers
       Salt           Transferrin
                        – Serum


       pH             Lactoferrin
                        – Saliva, milk, mucus


                       Defensins
       Lysozyme
                        – Mucus and
                          Extracellular fluid
                        – Lyse microbial cells

                                                 5
Cellular Defenses - Granulocytes
       Basophils/Mast cells         Neutrophils
        – Histamine release           – Early phagocytic cells
        – Inflammatory response




       Eosinophils                  Dendritic cells
        – Modulate inflammation       – Phagocytic
        – Peroxide release            – Antigen presenting
                                        cells, role in adaptive
                                        immunity

                                                                  6
Cellular Defenses — Agranulocytes
       Monocytes                    Lymphocytes
        – Phagocytic cells            – Cells of adaptive
        – Later appearance than         immunity
          neutrophils                 – Will be discussed in
                                        Ch. 17




                                                               7
Blood Cells




              8
Phagocytosis
      Cells Involved:
        – PMNs, macrophages, eosinophils
      Steps involved
        – Chemotaxis
            • Toll-like receptors on phagocytes (TLRs)
            • Recognition of microbial surface molecules
            • Cytokines, complement substances from damaged host cells
        – Adherence
            • Capsules, M proteins reduce this
            • Complement proteins enhance this
        – Ingestion
            • Formation of phagosome
        – Digestion
            • Phagosome + Lysosome = Phagolysosome
                 – Formation inhibited by P. falciparum
            • Enzymes and reactive oxides damage microbes
                 – Capsule protects microbes like Y. pestis
                 – Staph. Strep. release WBC degrading toxins - Leukocidins
                                                                              9
Phagocytosis Figure




                      10
Characteristics of Inflammation
      Cardinal signs:
       – Heat, Redness, Pain, Swelling
      Acute Inflammation
       – Vasodilation
       – Phagocytosis
       – Repair/regeneration
      Chronic Inflammation
       –   Continuous pus formation
       –   Healing never achieved
       –   Granulomatous tissue (gummas, tubercles, lepromas)
       –   Steroidal anti-inflammatories can release microbes from
           granulomas


                                                                     11
12
Fever
      Exogenous Pyrogens
        – Endotoxins, some exotoxins
      Endogenous Pyrogens
        – Interleukin 1 (IL-1)
      Benefits/Risks
        – Too hot for some microbes to grow, toxins may
          inactivate
        – Increase in interferon, phagocytosis, immune resonse,
          transferrin, lysosomal activity
        – Patients will rest
        – Convulsions, cardiac stress, dehydration may occur
          with v. high fevers
      Leukocyte Endogenous Mediator
        – Affects iron storage
                                                                  13
Interferons (IFN)
     Type I
      –   IFN-α
      –   IFN-β
      –   Antiviral
      –   Adjacent uninfected
          cells affected
     Type II
      – IFN-γ
      – Antiviral,
        antibacterial, anti-
        tumor
      – NK,T cells,
        macrophages
        affected
                                14
Complement Proteins
   Serum proteins
    (10% by weight)
   Activated by
      – Ag/Ab
        complexes
        (Classical)
      – Ag on pathogen
        surface
        (Alternate)

                         15
Complement System
     Activation leads to
      – Cytolysis of microbial
        cells
      – Increased inflammation
      – Opsonization
     Rapid effects
     Before immune cells
     Esp. alternate
      pathway


                                 16
Complement — Cytolysis




                         17
Non-specific
Defenses




               18

				
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posted:8/5/2011
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