Blood 2 Flashcards
how do neutrophils kill?
respiratory burst
what are the ROIs
suerpoxide anion, hydroxyl radical, hydrogen peroxide, hypochlorous acid
where does hypochlorus acid come from
from H2O2 by action of myeloperoxidase from azurophilic granules, produces hypochlorite (bleach)
what catalyzes the first step of the respiratory burst
NADPH oxidase
do phagosome membranes have NADPH oxidase
yes derived from plasma membrane
chronic granulomatous disease
involving any of the oxidase subunits
decreased or absent respiratory burst
recurrent bacterial and fungal infections
shorted life expectancy
specific granules contain
neutrophil
lysozyme: attacks cell walls of bacter, gram +
lactoferrin: competes with bacteria for iron and copper
collagenase: degrade ECM, easier access for neutrophil
azurophilic granules contain
neutrophil
myeloperoxidase: produces bleach
bactericidal/permeability-increasing protein (BPI): damages membranes of gram -
lysozyme
defensins: permeabilize bacterial membranes
neutrophil elastase: digest ECM
Chediak-Higashi syndrome
interferes with targeting of proteins to azurophilic granules, abnormally large vacuoles from fusion of azurophilic granules
don’t have mediators to kill bacteria
neutrophil extracellular traps (NETs)
strands of neutrophil chromatin with antimicrobial granule proteins
released from activated neutrophils
microbes stick and killed by high local concentrations of antimicrobial agents
help keep microbes from spreading
minimize local tissue damage
sepsis: NETs from within blood vessels
preeclampsia: form in intervillous spaces of placenta
require NADPH oxidase activity
how can neutrophils damage healthy tissue
elastase from azurophilic granules
collagenase from specific granules
release can occur during NET formation or phagocytosis
granules may fuse with phagosomes before it pinches off completely
what is pus and why is it green
dead neutrophils (necrotic death) green because of myeloperoxidase
how is pus removed
by macrophages
in what process are neutrophils important and what are 2 clinical indicators
important in acute inflammation
- leukocytosis: increased number, release of greater than normal numbers of neutrophils from bone marrow
- shift to the left: mature stores depleted, immature precursors released, shifts curve of nuetrophil age distribution
time course of an acute inflammation
- edema, leaky vessels by histamine
- neutrophils arrive during first wave, acute phase
- secrete chemotactic factors
- monocytes arrive, differentiate into macrophages, typical in late stage acute inflammation
- they phagocytize dead neutrophils, damaged tissue and other debris
extent of nuclear lobulation
neutrophil, eosinophil, basophil
neutro: 2-5 loves, thin strands
eosino: 2-3 lobes, thicker and/or shorter strands
baso: 2 poorly defined lobes
size and staining affinity of specific granules
neutro, eosino, baso
neutro: small, poorly staining
eosino: large, eosinophilic (pink to red)
baso: large basophilic (very dark purple)
specific granules of basophils
difficult to preserve, varied appearances
contents homogenous or grainy
may look like layers of membranes arranged in parallel stacks or whorls called myelin figures
basophil activation
involves IgE, made by plasma cells and binds to basophil receptors
primed but not activated
activated when exposed to antigen again and it binds to IgE causing it to cross-link