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Immunology > 51-Inflammation and Phagocytosis > Flashcards

51-Inflammation and Phagocytosis Flashcards

1
Q

what is the hallmark of the activation of the innate immune response

A

inflammation

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2
Q

how is inflammation activated

A

release of inflammatory mediators

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3
Q

what are the signs of inflammation

A 
redness
heat
swelling
pain
loss of function
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4
Q

what are the functions of inflammation

A

recruit immune cell
enhance immune cell function
limit spread of infection
promote tissue repair

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5
Q

what are the steps of inflammation

A

1-tissue damage causes release of inflammatory molecules because sentinel cells and pattern recognition receptors recognize pathogens
2-vasodilation to increase blood flow to damaged area and increase immune cells
3-blood clots localize the infection, abscess forms
4-promote wound healing

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6
Q

what does vasodilation cause during inflammation?

A

redness, swelling, pain, loss of function

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7
Q

how does fever response help infection?

A

decrease viability of pathogen

increase immune cell function

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8
Q

what are the sentinel cells

A

macrophages and mast cells

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9
Q

what do sentinel cells do

A

recognize pathogens and release inflammatory molecules

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10
Q

what are the inflammatory molecules and what do they do?

A

cytokines, chemokines, lipid mediators
1-vasodilation of blood vessels
2-recruit immune cells
3-activate immune cells

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11
Q

where are mast cells found

A

epithelial and mucosal layers

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12
Q

where are macrophages found

A

everywhere in the body

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13
Q

what do cytokines released by sentinel cells do

A

TNF, IL-1, IL-6, IL-12, IFN-gamma

enhance immune cell function, regulate vascular permeability

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14
Q

what are the important cytokines released by sentinel cells

A

TNF, IL-1, IL-6

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15
Q

what do lipid mediators do

A

alter vascular permeability, vasodilation, contraction of smooth muscle

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16
Q

what does histamine do

A

increase vascular permeability, increase vasodilation, increase pain responses

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17
Q

how does recruitment infection work

A

1-TNF and IL-1 are released from mast and macrophages to alter blood vessel endothelium. decreased cell to cell contacts and increase permeability
2- E and P selectin on vessel bind selectin ligand on cell to slow it down and roll
3-chemokine on vessel bind chemokine ligand on cell to activate integrin
4-integrin on immune cell bind integrin ligand on vessel (iCAM-1) to stop the cell
5-cell moves across vessel to infection

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18
Q

How does TNF work systemically

A

stimulate adipose and muscle for stored energy (immune system requires lots of energy)

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19
Q

How does the liver promote immunity systemically

A

release acute phase reactants after IL-1 and IL-6 stimulate

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20
Q

what do acute phase reactants do?

A

immunity and wound healing

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21
Q

what is C reactive proteins

A

an acute phase reactant used as a clinical marker for inflammation

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22
Q

when is inflammation good?

A

localized

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23
Q

when is inflammation bad?

A

systemically

24
Q

systemic inflammation can lead to what?

A

widespread vasodilation, low blood pressure, edema, collapse of blood vessels and organ failure and death

25
Q

high fever can lead to what

A

respiratory and CV disease, fatal

26
Q

what is the positive control feedback for inflammation

A

TNF and IL-1

27
Q

what are the negative feedback for inflammation

A

IL-1Ra to inhibit IL-1
soluble TNF receptors
immune suppressants cytokines TGF-B and IL-10

28
Q

what is DIRA and symptoms

A

lack of IL-1Ra, skin pustules, widening and lesions of bones

29
Q

treatment for DIRA

A

anakinra- recombinant IL-1Ra

30
Q

what is phaocytosis

A

ingestion and killing of microbial pathogens

31
Q

what is the purpose of phagocytosis

A

1-remove and kill pathogens
2-induce inflammation
3-activation of adaptive immune response

32
Q

what are the cells involved in phagocytosis

A

neutrophils, macrophages, dendritic cells

33
Q

characteristics of neutrophils

A

most abundant phagocytic cell
short lived (4-8 bacteria), rapidly migrate to infection
phagocytose and kill microbe
die by apoptosis quickly and leave behind remnants (pus)

34
Q

characteristics of macrophages

A

derived from monocytes
long lived found in tissues (Kaupffer, microglia, skin)
phagocytose and kill pathogens, induce inflammation, wound healing

35
Q

characteristics of dendritic cells

A

derived from monocytes
reside in tissues
process pathogens and present to t cells to activate adaptive response, wound healing

36
Q

when are macrophages used during infection

A

very early (sentinel), sense infection and induce inflammation, and later phases for wound healing

37
Q

when are neutrophils used during infection

A

early phases

38
Q

steps in phagocytosis

A 
1-migration/chemotaxis to infection
2-ingestion of pathogen into phagosome
3-fusion with lysosome granules to form phagolysosome
4-degradation of pathogen
5-release of debris
39
Q

what are the 2 cell surface proteins and what do they do

A

Innate immune receptors
opsonin receptors
adhere to pathogens and engulf them

40
Q

what do the innate immune receptors do?

A

bind directly to the pathogen ( mannose receptor binding mannose) to engulf pathogen

41
Q

what do the opsonin receptors do

A

bind to host protein to interact with pathogen (requires intermediate) CR3, CR4, Fc receptors

42
Q

what are the complement receptors and what do they bind to

A

CR3 and CR4 bind to complement fragments that are bound to the pathogen
Fc receptors which bind to antibodies bound to the pathogen

43
Q

how do phagocytic cells engulf apoptotic cells

A

apoptotic cells have changes in membrane
phosphatidyl serine is on the outside of the cell instead of the inside and is recognized by opsonin and innate receptors on macrophages. NON INFLAMMATORY. necrosis is inflammatory

44
Q

what are the 2 types of granules in phagocytes and what do they do

A

primary and secondary

degrade microbes and apoptotic cells

45
Q

what do primary granules do

A

resemble lysosomes and contain anti microbial proteins

46
Q

what do secondary granules do

A

activation of NADPH oxidase that form ROS

47
Q

what is different about the granules in macrophages vs. neutrophils

A

neutrophils have preformed granules that are functional

macrophages need to be activated by interferon gamma

48
Q

what activates macrophages granules

A

interferon gamma

49
Q

how does NADPH oxidase complex form

A

activation of Rac2 by opsonin or innate receptors
Rac2 binds gp91
gp91 recruits other subunits to form complex

50
Q

what does the NADPH complex do

A

use oxygen and NADPH to form free radicals. processed to hydrogen peroxide and hypochlorite

51
Q

how are nitrogen free radicals formed

A

by phagocytic cells using arginine, oxygen and NADPH

52
Q

what do nitrogen free radicals do

A

disrupt enzymes or form with more oxygen free radicals to alter tyrosine residues

53
Q

what are the symptoms of leukocyte adhesion deficiency

A

skin infections without pus, no loss of umbilical cord, recurrent infections. do not form abscesses.
poor migration of leukocytes to site of infection

54
Q

how do you treat leukocyte adhesion deficiency

A

bone marrow transplant

55
Q

what causes leukocyte adhesion deficiency type 1

A

defect in integrin on cell, cell doesn’t stop at infection

56
Q

what causes leukocyte adhesion deficiency type 2

A

defect in selectin ligands, cell doesn’t roll on vessel but it moves too fast past

Immunology (19 decks)

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