week 2- acute inflammation Flashcards
2 types of immune responses
innate, adaptive
main differences between innate and adaptive
innate: always ready, recognizes broad group of threats, does not have memory
adaptive: highly specific, recognize specific molecules, memory
players involved in innate immunity
macrophage, dendritic cell, neutrophil, eosinophil, mast cell, NKC
what are the 5 R’s
- recognition
- recruitment
- removal
- regulation
- resolution
c3 of the complement system results in what 3 actions?
- recruitment of neutrophils and monocytes
- opsonization for phagocytosis
- membrane attack complex
What is involved in recognition in innate immunity
PRR and PAMPs/DAMPs
What do PRR bind to ?
PAMPs/DAMPs
Where are PRR located
surface of cell, inside cell membrane, or soluble
How does Recognition of innate immunity work?
If pathogen sensed, PRR binds to it and produces cytokines and interferons which tell the body to produce immunity/reaction
an example of innate immunity recruitment
neutrophil recruitment
how does recruitment of innate immunity work?
-the cytokines will act on the endothelium of blood vessel and inflammatory cells.
-mast cells will release granules and histamine when sense danger or bind complement
-histamine stimulates inflam cells which react and allow the appropriate cells to move to the site of insult
4 steps of neutrophil recruitment
- margination
- rolling
- firm adhesion
- transmigration
3 main killing mechanisms of innate immunity removal?
intracellular killing
extracellular secretion and effectors
direct cell mediated killing of damaged/infected cells
example of intracellular killing
phagocytosis
4 steps of phagocytosis
1.detect
2. receptor signaling
3. internalization
4. destruction
3 parts of extracellular secretion and effectors
- degranulation
- contents of granules released into extracellular space
- neutrophil extracellular traps
what is involved in degranulation
neutrophils, eosinophils, mast cells
what is involved when the contents of granules are released into extracellular space?
-defensins
-proteolytic enzymes
-deployed inside PMN by fusion with phagosomes
-deploy extracellularly as well
what is involved in a Neutrophil extracellular trap?
-composed primarily of neutrophil DNA
-binds pathogens
-disarm them with antimicrobial proteins
-physical barrier
-minimize damage to host cells
what is involved in direct cell mediated killing of damaged/infected cells?
control of natural killer cells
what are natural killer cells
-perforin forms pores in plasma membrane
-granzyme enters via perforin pores
-activates apoptosis, cleaves many things
-very controlled
how do we control NKCs
remove the inhibitor and bind the activator to release killing enzymes
2 categories of inflammation
acute, chronic
what happens during acute inflammation
-dilation of small blood vessels
-increase vascular permeability
-emigration of leukocytes
-minutes to days
what happens during chronic inflammation?
-infiltration with mononuclear cells
-tissue destruction
-attempts at healing
-days to years
what are cardinal signs of inflammation?
-rubor
-tumor
-calor
-dolor
-functio laesa
what part of acute inflammation is the fluidic phase
- dilation of small blood vessels
- increased vascular permeability
what part of acute inflammation is the cellular phase
- emigration of leukocytes from vasculature
what happens during dilation of small blood vessels?
-changes in blood
-vasodilation (involves arterioles, opening of new capillary beds)
-results in increased blood flow (erythema)
what happens during increased vascular permeability?
-hallmark of acute inflammation
-post capillary venules
-allows plasma proteins and leukocytes to reach sites of infection
-early fluid leakage is low protein, low cellularity
-both increase as response increases
what are mechanisms of vascular permeability
retraction of endothelial cells
endothelial injury
leukocyte mediated vascular injury
increased transcytosis
what happens during vasodilation microvascular permeability
-loss of fluid and increased vessel diameter
(-results in slower blood flow
-conc of red cells
-increased blood viscosity)
-leads to venous stasis -congestion (redness)
-leukocytes come out of laminar flow to contact endothelium
what causes redness and heat in acute inflammation?
vasodilation, stasis, hemoconcentration
what is transudate?
-extravascular fluid with low protein content, low SG, and few cells
-clear, thin, effusions, and edema
what causes transudate fluid leakage?
leaky vessels
retraction of endothelial cells
due to increased histamines
what is exudate protein leakage?
endothelial gaps get bigger and more proteins and cells leak out making the fluid more cloudy and viscous
-low protein, SG, and increased cells
what is fibrin?
-an insoluble protein formed from fibrinogen during the clotting of blood, it forms a fibrous mesh that impedes the flow of blood
-made in liver
-forms friable, threads, and plaques during acute inflammations
how is fibrin formed
thrombin cleaves fibrinogen to fibrin
what components occur during the cellular phase of acute inflammation (recruitment) ?
-deliver leukocytes to site of injury
-allows for removal
-leukocyte adhesion cascade
what is involved in leukocyte adhesion cascade
margination
rolling
stable (tight) adhesions
transmigration
what is cellular exudate?
-viscous, opaque
-may have flecks of fibrin, pockets of fluid
-cells recruited to site of injury
-can remove damage
-neutrophils=pus, suppurative
what causes redness
increased blood flow and vascular permeability
what causes heat
increased blood flow
what causes swelling
edema, and cell accumulation
what causes pain
damage to tissue, release of mediators of inflammation
what causes loss of function
due to pain and tissue damage
