Flashcards in 51-Inflammation and Phagocytosis Deck (56)
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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
