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