Chapter 16: Innate Host Defenses Flashcards
Adaptive host defense
Specific: responds to particular antigens
- acquired after exposure to antigen
Antigen
Molecule identified as foreign
Innate host defense
Non-specific: genetic defense that acts against any invading pathogen
- necessary to start adaptive defense
Types of innate defenses
Physical barriers Chemical barriers Cellular defenses Inflammation response Fever response Molecular defenses
Physical barriers
Skin: thick layer of cells
Keratin strengthens skin cells
Mucous membranes
Chemical barriers
pH: sweat and sebum are acidic, which is antibacterial (ex: gastric acid in stomach)
Salt: sweat used osmotic pressure to draw water out of the bacteria
Lysosyme: enzyme that prevents peptidoglycan synthesis (in mucous, saliva, tears, body secretions)
Cellular defenses
White blood cells (leukocytes)
- Granulocytes
- agranulocytes
Granulocytes
Visible granules in cytoplasm and lobed nuclei
- Basophils: release histamine, involved with inflammation and have a role in allergies
- Eosinophils: role in allergies and worm infections
- Neutrophils: phagocytes = engulf and digest pathogens and debris
- Dendritic cells: phagocytes that play a role in adaptive immunity
Agranulocytes
No granules and round nuclei
- monocytes: mature into macrophages (big eaters), which are phagocytes
- lymphocytes: B and T lymphocytes - adaptive immunity
- natural killer lymphocytes: attack abnormal cell nonspecifically (ex. virus infected)
Phagocytosis
- Chemotaxis: phagocyte is drawn towards chemicals released by the pathogen or damaged tissue
- Adsorption/adherence: phagocyte attaches to pathogen
Ingestion: phagocyte engulfs pathogen into phagosome - Digestion: lysosomes with digestive enzymes fuse with phagosome
- Excretion: release of undigested material through exocytosis
Inflammation
Body’s way to clean up infected/damaged tissue to set up area for healing
Cardinal signs of inflammation
Calor: increase in temperature
Rubor: redness
Tumor: swelling
Dolor: pain
Stages of acute inflammation
- Vasodilation: blood vessels are dilating to bring more blood to the area (^temp, ^redness)
- Increase in vessel permeability: blood vessels leak fluid into tissues (^swelling, ^pain)
- Phagocytosis: chemotaxis to damages area, engulf and digest pathogens and debris
- Tissue repair: pus may form, dead WBCs, debris
Chronic inflammation
Continuous pus formation, no tissue repair (can lead to permanent tissue damage)
- cause granulomas
Granulomatous tissues
Walled off pockets of inflammation
- gumma: permanent tissue damage, syphilis causes gumma in brain and skin
- leproma: leprosy disfigures skin or nerves
- tubercle: tuberculosis causes lesions in lungs
Fever response
Systemic increase in body temperature
- goal is to raise body temp above pathogens optimal temp to cause denaturation of pathogen
Pyrogens
Chemicals that cause fever
- exogenous: come from outside of your body, pathogens
- endogenous: WBCs may release chemicals to induce fever
Benefits of fever
- reduced microbial growth
- toxin inactivation
- increased phagocytosis
- increased metabolism and immune cell response
- rest for patient
Molecular defenses
Interferon
Complement
Interferon
Protein synthesized by a virus infected cell to tell nearby cells to make the antiviral protein
- interferes with a virus being able to infect and replicate
Interferon mechanism
- Virus infects cell
- Infected cell makes interferon
- Interferon binds to surface of neighboring cells
- Cell is stimulated to make antiviral proteins
- Antiviral proteins block viral replication
Complement
A series of ~26 proteins that cascade in reactions
- enhance inflammation
- opsonization
- membrane attack complexes
Opsonization
Coats pathogen with protein (often antibodies) that enhance the adherence step in phagocytosis
MACs
Create holes in pathogen membrane which cause it to lyse
