1 Host Defenses Adaptive Innate

2 Defense Barriers Physical Chemical Cellular defenses Inflammation Fever Molecular defenses

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

4 Chemical Barriers Salt pH Lysozyme Transferrin Lactoferrin Defensins

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

6 Cellular Defenses — Agranulocytes Monocytes Lymphocytes

7 Phagocytosis Cells Involved: 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

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

9 Fever Exogenous Pyrogens Endogenous Pyrogens 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

10 Interferons (IFN) Type I Type II

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