BIOL 4124 : Test 2 Study Guide
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Innate Immunity
1. What are innate immune defenses?
a. first line of defense against microbes
2. What are innate immune defenses based on?
a. Based on biochemical differences between microbes and host cells
3. What is another name for innate immune defenses? Why is it called that?
a. responds to entire group of similar microbes in the same manner-
“nonspecific”
4. What are some barriers to infection?
a. Skin, mucosal membranes
5. How does skin protect against infection?
a. Generally inhospitable to foreign microbes
i. Cool, dry, acidic (pH 5.0)
ii. Dead layer of cells on top provides an “armor”
iii. antimicrobial oil (sebum)
iv. antimicrobial swear secretions
b. Normal flora colonize the skin and can “crowd out/starve out” potential
invaders
6. How do mucosal membranes protect against infection?
a. Interior surfaces coated with wet mucus
i. Moves along the surface to prevent microbe attachment
ii. Contain antimicrobial molecules
1. Defensin proteins
2. Lysozyme
b. Competitive exclusion by normal flora
7. What is inflammation?
a. Physiologic response to microbial invasion and damage
8. What is inflammation triggered by?
a. Triggered by release of proinflammatory molecules (such as histamine and
cytokines) from local cells
9. What are some examples of proinflammatory molecules?
a. (such as histamine and cytokines)
10. What are the steps of the inflammatory response?
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a.
11. What are some consequences of local inflammation?
a. Vasodilation
b. Extravasation – movement of white blood cells to the damaged tissues
c. Increase in permeability of vessels
12. What is the purpose of inglammation
a. bring in immune cells (e.g.,phagocytes) to fight the infection
13. What are cytokines?
a. Chemical mediators that communicate the status of an infection and let
immune cells know that there is something wrong. Chemical alarm signals
14. What are some examples of cytokines?
a. (interleukins, tumor necrosis factor, etc)
15. What molecule communicates the status of an infection?
a. Cytokines
16. Side effect of cytokine signaling?
a. Sore – bradykinins
b. Hot
17. What is systemic inflammation?
a. If inflammation gets out of hand, it can be damaging
b. can happen when microbes or their products get into the bloodstrem
18. What is septic shock?
a. Widespread presence of bacteria in the body induces system-wide
inflammation.
19. What is toxic shock?
a. Overstimulation of immune responses by toxins in the blood
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20. What is the prognosis for systemic inflammation
a. Death rates 30 – 50%
Molecules of the Innate System
21. What are complement proteins?
a. group of 30+ serum proteins
b. involved in antimicrobial activities
22. Activation of complement proteins results in?
a. Inflammation
b. Opsonization (enhancing phagocytosis)
c. Direct microbe killing by formation of membrane-attack complex (MAC)
23. How does complement work?
a.
b. As long as complement is not activated proteins stay separated. They don’t
react with each other. If something (say an infection) cuases them to be
activate, then once they are activated that causes
i. Increase inflammation
ii. Help w/ phagocytosis (Opsonization)
24. How does opsonization work?
a. Bacteria has complement protein bound. Complement protein can also bind
to a receptor on the phagocyte and when it does, it basically delivers the
bacterial cell to the phagocyte. Phagocyte can more easily engulf it.
b. Complement can bring bacteria and phagocyte together, since it can bind
both at the same time.
25. Why can’t complement proteins directly kill Gram + bacteria?
a. Cell wall is usually too thick to penetrate.
26. How do complement proteins directly kill Gram - bacteria
a. Gram – complement will form pores in the cell envelope complex. Cell
contents like out through pores and the cell dies.
Document Summary
What are some barriers to infection: how does skin protect against infection, skin, mucosal membranes. Nonspecific : dead layer of cells on top provides an armor , cool, dry, acidic (ph 5. 0, generally inhospitable to foreign microbes. 1: what are some consequences of local inflammation, vasodilation. Extravasation movement of white blood cells to the damaged tissues. 2: what is the prognosis for systemic inflammation, death rates 30 50% Inflammation: opsonization (enhancing phagocytosis, direct microbe killing by formation of membrane-attack complex (mac, how does complement work, as long as complement is not activated proteins stay separated. If something (say an infection) cuases them to be activate, then once they are activated that causes: increase inflammation, help w/ phagocytosis (opsonization, how does opsonization work, bacteria has complement protein bound. Complement protein can also bind to a receptor on the phagocyte and when it does, it basically delivers the bacterial cell to the phagocyte.
