Inflammation 1 & 2
acute
stimuli
toxins
trauma
physical and chemical inflammation
any kind of tissue necrosis
foreign bodies
hypersensitivity
immune reactions
suture material
splinters
phases
heat
redness
swelling
pain
loss of function
3 sequential phases
- fluidic (dilute it)
- cellular (destroy it)
- reparative
infections
immediate and early response to tissue injury
endogenous and exogenous injury
hyperermia
step 1: vasodilation
redness and heat
chemical mediators
where they come from
classes
changes in jxn'l complexes of endothelial cellls
leakage of fluid
transudate
exudates
balanced e- solution
blister, sunburn
no cells
no proteins
protein rich
opaque
short-lived histamine response
increased vascular permeability
structural recorganization of cytoskeleton
edema
IL-1, TNF, IFN-y
can't go too far
leukocyte arrival
destructive enzymes
free O radical production
increased transcytosis
VEGF
increased channels
indicating immune response
fibrinogen rich
triple response of flush, flare, weal
plasma-derived
cell-derived
compement
kinins
coag factos
mast cell histamine
NO
qualities
short half lives
enzymatically destroyed
scavenged by antioxidants
blocked by endogenous inhibitors
vasoactive amines
plasma proteins
arachidonic acid
cytokines, including chemokines
oxygen-derived free radicals
histamine
mast cells in response to
IgE
C3a
C5a
serotonin
platelets
histamine-like actions
kinin system
bradykin
vasoactive peptide
10x more potent than histamine
pain
complement system
anaphylatoxins
stimulate histamine
C5a
C3a
chemotaxis
C3b
opsonization
clotting system
thrombin (factor IIa)
coagulation cascade
released from membrane phospholipids
COX pathway
prostaglandins
thromboxanes
fever
hemostatis
tachycardia
lipoxygenase pathway
lipoxins
prostaglandins
PGI2
endothelial cell activation
actions
local actions
fibrous connective tissue production
sources
ctivated macrohpages
NK cells
endothelial cells
stimuli
LPS
Ag-Ab complexes
toxins
increase vascular permeability
IL-1
TNF-a
produced by endothelial cells, macrophages
smooth muscle relazation
vasodilation
counteract platelets
released by macrophages and neutrophils
damaging to surrounding cells and enzymes
leukocyte delivery
ingest offending agents
isolate and destroy
dilution
kill microbes
clear necrotic tissue and foreign substances
extravasation and phagocytosis
margination
rolling
adhesion
transmigration
chemotactic stimuli
leukocyte adhesion cascade
cells
endothelial cells
gap widening
cell contraction
cytoskeletal reorganization
injury
necrosis
detachment
leukocyte-induced
platelets
5-6 day lifespan
born in bone marrow
major component in hemostasis
release chemical mediators
cytokines
adhesion molecules
facilitate healing
neutrophils
usualy 1st to arrival at site of insult
short-half life
primary circulating WBC
20-30% circulating in ruminants
temporarily marginate
vasoactive amines
left shift
increase in proportion of immature cells
response to intense, acute inflammation
cytoplasmic granules
O2 dependent killing
O2 indepenent killing
bactericidal permeability increasing protein (BPI)
lysozyme
lactoferrin
adhesion molecules
composition varies by species
heterophils in avians, non-mammals
H2O2-MPO-chloride system
defensins
reactive O species
NADPH oxidase
myeloperoxidase
drilling holes in cell walls, etc.
tissue damage risk
mast cells
near small blood and ymphatic vessels in skin, mucus membranes
cytoplasmic granules
more resident cells
hang out close to potential breaches
usually aren't recruit in
histamine
heparin
enzymes
chemotactic factors
functions
late vascular events
lifespan of months
degranulation doesn't lead to death
proliferate in tissues
inflammatory mediator synthesis from arachidonic acid
cytokines
prostaglandins
early vascular events
leukotrienes
histamine
allergies, anaphylaxis
IgE receptors
parasite defense
ECM remodeling
immediate
vasodilation
increased vascular permeability
vasodilation
sustained vascular permeability
pain
stimuli
heat
cold
trauma
complemet fragments C5a,C3a
cytokines IL-1, IL-8
neutrophil enzymes
type I hypersensitivity
uticaria (hives)
eosinophils
toxic to parasites
live close to muscosal surfaces
cationic protein
eosinophil derived neurotoxin
aggressive to lipid membranes
prodce wide array of cytokines
functions
kill/damage parasites
hypersensitivity rxns/anaphylaxis
attracted by
mast cells
histamine
IL-5
C5a
eotaxin
short half life
mobile, can go after parasites
dirt
examples
serous
fibrinous
suppurative
polymerizes to form fibrin
inital would healing framework
traps microorganisms
isolates stimulus
prostaglandins
think of allergic responses
leukotrienes
vascular permeability
chemotaxis
vasoconstriction
systemic actions
neutrophil activation
IFNy
priduced by lymphocytes
stimulated by virus, parasites, neoplasms
activate NK cells and macrophages
serotonin
growth factors
major basic protein
uses peroxidase for oxidative burst