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BIO 669 EXAM 1. 150 ACTUAL EXAM QUESTIONS WITH VERIFIED CORRECT ANSWERS. LATEST €11,04
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BIO 669 EXAM 1. 150 ACTUAL EXAM QUESTIONS WITH VERIFIED CORRECT ANSWERS. LATEST

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BIO 669 EXAM 1. 150 ACTUAL EXAM QUESTIONS WITH VERIFIED CORRECT ANSWERS. LATEST

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  • 9 augustus 2024
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BIO 669 EXAM 1. 150 ACTUAL EXAM QUESTIONS WITH
VERIFIED CORRECT ANSWERS. LATEST 2024-2025

1. Cytokines: signaling molecules that regulate innate or adaptive immunity that are
responsible for activating other cells and regulating the inflammatory response; they help
stimulate the response to infection and tissue damage by guiding lymphocytes and
leukocytes toward the area of damage, stimulating healing, and increasing or decreasing
inflammation; there are multiple types of these cells, each with their own different roles
in the inflammatory response
2. Chemokines: type of cytokines that are synthesized by many cells in response to
proinflammatory cytokines and induce chemotaxis to promote phagocytosis and wound
healing; e.g. monocyte/macrophage chemotactic proteins, macrophage inflammatory
proteins, and neutrophils
3. Cells that synthesize chemokines: macrophages, fibroblasts, endothelial cells
4. Interleukins: type of cytokine made by white blood cells (produced primarily by
macrophages and lymphocytes) in response to stimulation of pattern recognition
receptors (PRRs) or by other cytokines; there are many different types of these cytokines
5. Interleukin-1: pro-inflammatory cytokine (activates and enhances inflammatory
response) that induces many acute phase proteins and is an endogenous pyrogen
6. Endogenous pyrogen: molecule that stimulates fever by resetting the hypothalamic
set point, setting the body's temperature set point higher so that initially you feel cold as
your body temperature as risen, but then as the fever breaks and your temperature goes
back down, you feel hot
7. Interleukin-10: anti-inflammatory cytokine that is primarily produced by
lymphocytes and suppresses the growth of other lymphocytes and the production of
proinflammatory cytokines of macrophages, which leads to a down-regulation of both
inflammatory and acquired immune response
8. Tumor necrosis factor-alpha: cytokine secreted by macrophages in response to
PAMPs and toll-like receptor recognition that is a strong inflammatory mediator and a
key regulatory molecule for inflammation; induces a multitude of proinflammatory
effects
9. Effects of tumor necrosis factor-alpha: - Induces fever by acting as an
endogenous pyrogen (also produces IL-1 and IL-6, which can also both induce/increase
fever)
- Increases synthesis of inflammatory serum proteins
- Causes muscle wasting (cachexia) and intravascular thrombosis
- Can cause granuloma formation






,10. TNF-A and biologic agents: tumor necrosis factor alpha is the target of many
biologic agents that try to diminish the immune response when it is overexpressed/out of
proportion; since TNF-A enhances inflammation, drugs that target TNF-A will ramp
DOWN the inflammatory response; e.g. used in treatment of rheumatoid arthritis,
psoriatic arthritis, Crohn's disease (autoimmune conditions where immune system is too
active)
11. Interferon: cytokine that protects against viral infections and modulate the
inflammatory response
12. Interferons alpha and beta: Type I interferons that are produced and released by
virally infected host cells in response to viral double-stranded RNA and other viral
PAMPs to protect neighboring healthy cells; don't kill viruses directly
13. Interferon gamma: Type II interferon that is produced primarily by lymphocytes
to activate macrophages, which results in increased capacity to kill infectious agents like
viruses (and bacteria); key cytokine; increases microbicidal activity of macrophages
- Plays important role in how well you can clear infection
14. Mast cells: white blood cells that are the most important cellular activator of the
inflammatory response; cellular bags of granule
- located in the loose connective tissues close to blood vessels (skin, digestive lining, and
respiratory tract)
- their granules contain histamine, cytokines, serotonin, and chemotactic factors that
when released, can lead to a significant inflammatory response -
mediator for pollen, allergic rhinitis, hay fever, etc.
15. Degranulation of mast cells: most common activation of mast cell chemical release
- the release of the contents of the mast cell granules (histamine, serotonin, chemotactic
factors, cytokines, etc.) in response to a receptor being engaged that allows for the
stimulation of mast cells
- this receptor is frequently an antibody acting as a receptor (e.g. IgE)
- IgE binds to mast cells, causing them to release and produce a very strong, immediate,
acute immune response (e.g. allergic asthma and other allergic responses)
16. Basophils: granulocyte found in the BLOOD that most likely act the same way as
mast cells
- least prevalent granulocyte
- primary role unknown
17. Synthesis: method of mast cell release in which mast cells produce and release
new mediators in response to a stimulus
18. Histamine: chemical stored in mast cells and is released during degranulation that
is a vasoactive amine (many vascular effects) and causes:
- temporary, rapid constriction of the large blood vessels





, - dilation of the postcapillary venules (resulting in increased blood flow into the
mcirocirculation)
- increased vascular permeability due to the retraction of endothelial cells lining the
capillaries
- allows fluid and proteins to leave the vasculature, leaking out into tissues, which causes
redness, swelling, pain, loss of function, etc. (inflammation!)
19. Why do antihistamines not reduce all inflammation?: Antihistamines can
reduce some inflammation (the vascular effects caused by histamine), but histamine is
not the only mediator released by mast cells. These mediators also have inflammatory
effects, so they cannot treat all of the effects of inflammation, only the ones caused by
histamine.
20. Neutrophil chemotactic factor and eosinophilic chemotactic factor of
anaphylaxis: chemotactic factors contained in mast cell granules and released during
degranulation that attract eosinophils and neutrophils, promoting inflammation
21. Phopholipase A2: mast cell synthesis can stimulate the production of this enzyme,
which takes the phospholipids from many cell membranes an dconverts them into
arachidonic acid and platelet activating factor
22. Arachidonic acid: molecule that is broken down/metabolized into cyclooxygenase
and 5-lipoxygenase; these metabolites play key roles in inflammation
23. Cyclooxygenase: enzyme that produces prostaglandins from arachidonic acids;
targeted by NSAIDs to stop inflammation due to prostaglandins (e.g. pain, inflammation)
24. Prostaglandins: fatty acids that are produced from arachidonic acid via
cyclooxygenase that cause increased vascular permeability, neutrophil chemotaxis,
and pain by direct effects on nerves
25. 5-lipooxygenase: enzyme that produces leukotrienes from arachidonic acid
26. Leukotrienes: - produced from arachidonic acid from 5-lipooxygenase - play a role
in anaphylaxis
- have vascular effects (increased vascular permeability), like histamine
- cause smooth muscle contraction (like histamine)
- affect the bronchial tree and mediate some of the responses seen in asthma
27. Why don't NSAIDs treat asthma/swelling in bronchi?: NSAIDs do not affect
swelling in the bronchi (i.e. in asthma) because bronchial swelling is caused by
leukotrienes, NOT prostaglandins! So, NSAIDs could actually make bronchial swelling
worse because when they block cyclooxygenase from converting arachidonic acid into
prostaglandins, they allow more archidonic acid to be converted into leukotrienes! =
increased bronchial swelling
28. H1 receptor: one of the receptors histamine can bind to that is proinflammatory and
located in the smooth muscle cells of the bronchi

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