CH 16 - Innate Immunity: Nonspecific defenses of the host Flashcards
Concept of Immunity
Susceptibility:
Resistance:
Immunity:
Susceptibility: ability to be productively infected
Resistance: unable to allow a productive infection
Immunity: an active process that prevents establishment or progression of infection
Lysozyme
a small enzyme that attacks the peptidoglycan chain in cell walls of bacteria, causing the cells to burst
Antibacterial substances
Sweat, saliva, sebum, urine
Lysozyme
sweat, tears, saliva
Leukocytosis
Increase in white cell count
Leukopenia
Decrease in white cell count
Neutrophils
Highest in white cell count
live only a short time
predominate early in infections
Macrophages
lasts up to several months
predominate later in infections
Phases of phagocytosis
The phases of phagocytosis:
- chemotaxis and adherence of pseudopods
- ingestion of target
- formation of phagosome
- fusion of phagosome with lysosome
- digestion of target by digestive enzymes
- formation of residual body
- discharge of indigestible material
Toll-like receptors
Toll-like receptors:
are protein molecules on cell surfaces throughout the body.
TLRs are how macrophages pseudopods adhere to bacteria.
TLRs recognize bacterially-produced molecules and signal the immune system via cytokines that bacteria are present.
How do Strep. pyogenes and S. pneumonia evade phagocytosis?
they inhibit adherence due to the presence of M proteins, capsules.
How do Staph. aureus evade phagocytosis?
they kill phagocytes due to the presence of leukocidins
How do Listeria monocytogenes evade phagocytosis?
they lyse phagocytes through membrane attack complex
How do Shigella, Rickettsia evade phagocytosis?
they escape phagosome
How do HIV, M. tuberculosis evade phagocytosis?
they prevent phagosome-lysosome fusion
How do Coxiella burnettii evade phagocytosis
survive in phagolysosome
During inflammation, what are the signal molecules released by cell damage and their functions?
Histamine & Kinin: vasodilation and increased blood vessel permeability
Prostaglandins: Intensify effect of Histamine & Kinin; fever
Leukotrienes: increased blood vessel permeability
what are the advantages of fever?
- Increases interleukin (IL-1) activity
- Increases transferrin
- Produces interferon
What are the disadvantages of fever?
Tachycardia; acidosis; dehydration; high temperature
Describe the steps in the classical pathway of component Activation
- C1 is activated by microbe-antibody complex
- C1 causes C2 to split into C2a and C2b
- C1 causes C4 to split into C4a and C4b
- C2a and C4b combines to split C3
- C3a and C3b initiate complement cascade
- C3b causes opsonization
- C3b also splits C5 into C5a and C5b
- C5b, C6, C7, C8, C9 forms membrane attack complex
- C3a and C5a causes inflammation
Which of the complement cascades present in classical pathway are not involved in alternative pathway
C1, C2, and C4. Instead, host proteins, B,D, and P bind to microbes and combine with C3 to activate it.
Lectin pathway of complement activation
C1 is not involved. Lectin binds to microbe and splits C2 and C4
Which interferons cause cells to produce antiviral proteins.
IFN-alpha and beta
Which interferon causes neutrophils and macrophages to phagocytize bacteria
IFN-gamma
