51-Inflammation and Phagocytosis Flashcards Preview

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Flashcards in 51-Inflammation and Phagocytosis Deck (56)
1

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

inflammation

2

how is inflammation activated

release of inflammatory mediators

3

what are the signs of inflammation

redness
heat
swelling
pain
loss of function

4

what are the functions of inflammation

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

5

what are the steps of inflammation

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

6

what does vasodilation cause during inflammation?

redness, swelling, pain, loss of function

7

how does fever response help infection?

decrease viability of pathogen
increase immune cell function

8

what are the sentinel cells

macrophages and mast cells

9

what do sentinel cells do

recognize pathogens and release inflammatory molecules

10

what are the inflammatory molecules and what do they do?

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

11

where are mast cells found

epithelial and mucosal layers

12

where are macrophages found

everywhere in the body

13

what do cytokines released by sentinel cells do

TNF, IL-1, IL-6, IL-12, IFN-gamma
enhance immune cell function, regulate vascular permeability

14

what are the important cytokines released by sentinel cells

TNF, IL-1, IL-6

15

what do lipid mediators do

alter vascular permeability, vasodilation, contraction of smooth muscle

16

what does histamine do

increase vascular permeability, increase vasodilation, increase pain responses

17

how does recruitment infection work

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

18

How does TNF work systemically

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

19

How does the liver promote immunity systemically

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

20

what do acute phase reactants do?

immunity and wound healing

21

what is C reactive proteins

an acute phase reactant used as a clinical marker for inflammation

22

when is inflammation good?

localized

23

when is inflammation bad?

systemically

24

systemic inflammation can lead to what?

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

25

high fever can lead to what

respiratory and CV disease, fatal

26

what is the positive control feedback for inflammation

TNF and IL-1

27

what are the negative feedback for inflammation

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

28

what is DIRA and symptoms

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

29

treatment for DIRA

anakinra- recombinant IL-1Ra

30

what is phaocytosis

ingestion and killing of microbial pathogens

31

what is the purpose of phagocytosis

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

32

what are the cells involved in phagocytosis

neutrophils, macrophages, dendritic cells

33

characteristics of neutrophils

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

characteristics of macrophages

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

35

characteristics of dendritic cells

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

36

when are macrophages used during infection

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

37

when are neutrophils used during infection

early phases

38

steps in phagocytosis

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

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

Innate immune receptors
opsonin receptors
adhere to pathogens and engulf them

40

what do the innate immune receptors do?

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

41

what do the opsonin receptors do

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

42

what are the complement receptors and what do they bind to

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

43

how do phagocytic cells engulf apoptotic cells

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

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

primary and secondary
degrade microbes and apoptotic cells

45

what do primary granules do

resemble lysosomes and contain anti microbial proteins

46

what do secondary granules do

activation of NADPH oxidase that form ROS

47

what is different about the granules in macrophages vs. neutrophils

neutrophils have preformed granules that are functional
macrophages need to be activated by interferon gamma

48

what activates macrophages granules

interferon gamma

49

how does NADPH oxidase complex form

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

50

what does the NADPH complex do

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

51

how are nitrogen free radicals formed

by phagocytic cells using arginine, oxygen and NADPH

52

what do nitrogen free radicals do

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

53

what are the symptoms of leukocyte adhesion deficiency

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

54

how do you treat leukocyte adhesion deficiency

bone marrow transplant

55

what causes leukocyte adhesion deficiency type 1

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

56

what causes leukocyte adhesion deficiency type 2

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