Host Defenses n Adaptive n Innate 1 Defense

Host Defenses n Adaptive n Innate 1

Defense Barriers n n n Physical Chemical n Inflammation n Fever n Molecular defenses Cellular defenses 2

Physical Barriers n Skin – Stratified – Close intercellular junctions – Waterproof, dead cells n Mucous membranes – Simple epithelium – Mucus layer 3

Chemical Barriers n Salt n Transferrin n p. H n Lactoferrin n Lysozyme n Defensins 4

Cellular Defenses - Granulocytes n Basophils/Mast cells n Neutrophils n Eosinophils n Dendritic cells 5

Cellular Defenses — Agranulocytes n Monocytes n Lymphocytes 6

Phagocytosis n Cells Involved: n 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 ________ – Digestion • _____ + ________ = ____________ – Formation inhibited by P. falciparum • Enzymes and reactive oxides damage microbes – Capsule protects microbes like Y. pestis – Staph. Strep. release WBC degrading toxins - Leukocidins 7

Characteristics of Inflammation n Cardinal signs: n Acute Inflammation n Chronic Inflammation – – Continuous pus formation Healing never achieved Granulomatous tissue (gummas, tubercles, lepromas) Steroidal anti-inflammatories can release microbes from granulomas 8

Fever n Exogenous Pyrogens n Endogenous Pyrogens n 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 n Leukocyte Endogenous Mediator 9

Interferons (IFN) n Type II 10

Complement Proteins Serum proteins (10% by weight) n Activated by n – Ag/Ab complexes (______-) – Ag on pathogen surface (______) n Activation leads to n Rapid effects, before immune cells are activated, esp. alternate pathway 11