Inflammation 4 Flashcards
in add’n to opsinins coating phagocytes, the neutrophil can also be triggered to engulf pathogens by
PAMPs on pathogens bindnig to PRR
CR3 and CR4 are
complement receptors
CR3 and CR4 bind to
C3B
IC3B
neutrophils have two types of granules
auzorophilic granules
specific granules
contained in the granules are
microbial substances
following delivery of the granules from neutrophils to phagosome we also get delivery of
lysosomal contents to phagosome
when lysosomes fuse with phagosome forms
phagolysosome
neutrophil after phagocytosis does what
dies - it exhausts itself
if infection isn’t resolved by neutrophils the
monocyte → macrophage and cleans up after neutrophil
part of specific granuels for killing in neutrophils is what coplex
NADPH oxidase complex
superoxide is reactive and can do what
damage to biomoleuless
superoxide dismutase converts 2O2- to
hydrogen peroxide
hydrogen peroxide converted by myeloperoxidase into:
HOCl (bleach!)
oxidative killing increases O2 demand by 100x so it’s called
respiratory burst
do resting neutrophils have NADPH complex
no they aren’t active in terms of oxidative killing
what are the non-oxidative killing list of neutrophils
Elastase
Cathepsins/other proteinases
Collagenase
Lactoferrin
“Cathy Elatedly Lactated in Collage”
which is most important killing mechanism for neutrophils
oxidative killing
in individuals without ability to form NADPH disease:
they are totally competent in non-oxidative killing mechansm
they have recurrent bacterial infections
memorize table on pg
87
monocyte differentiate into what in tissue
macrophage
how do monocyte get into infected tissue
same way as neutrophil
rolling
tight binding
pulled through gaps
monocytes and macroh[ages have what on surface
PRR - allows them to take up opsinized material and the bacteria or other pathogens that have glycoproteins on surface
receptors on surface of macrophage we need to know
pg 90 memorize
Mac-1, CD11b/CD18
pg 90
Dectin-1
allows fungi to be recognized and taken up - it binds to beta glucans (part of fungal cell wall)
macrophage has how many TLR
10 - can detect variety of pathogens
what is first to infiltrate infection
neutrophil
neutrophils are mobilized from
bone marrow
neutrophils once they do their job they will
die
the cell following neutrophil will
continue fighting or clean up dead neutrophils
monocyte → macrophage
cytokines that promote inflammation
IL-1, IL-6, IL-8, IL-12, Interferons, TNFs (TNF-)
IL12 and interferons are important in what response
innate respose against viral infections
once inflammatory response has done its job need what
IL-10 and TGF-β
IL-10 and TGF-β are
anti-inflammatory
IL-1, IL-6, TNF-a control
acute phase response
IL-1, IL-6, TNF-a iportant for promoting
acute phaseinflammation
interferons do qhat
Activate NK cells.
Provide anti-viral protection to neighboring cells.
IL is a
cytokine
IL-1 induces expression of
adhesion molecules on vascular endothelial cells
TNF alpha
shares with IL - 1 increases expression of adhesion molecules on vascular endothelial cells
allows recuirted leukocytes to roll on endothelial cells and halt when integrin has been activated by exposre of leukocyte to chemoattractant
induces production of acute phase protiens
induces sytokine secretion by inflammatory cells
Tumor Necrosis Factor-alph is
TNF alpha
TNF alpha important for controling
localized infection
systemic release of infection thats bad why
system production of TNF alpha will cause bulk movement of fluid from circulation into tissues
will lead to dramatic drop in blood pressure, collapse of blood vessels, which leads to disseminated intravascular coagulation which leads to oran failure
Disseminated intravascular coagulation leads to
organ failure