Chronic Inflammation Flashcards
how does our immune system recognize microbes/dead tissue?
toll like receptors
g-protein coupled receptors
opsonins (Ab, C)
cytokine receptors (IFN-y)
opsinization
coated microbes are targed for ingestion
Fc of IgG
C3b
collectin
recognitoin receptors
opsonin receptors
mannose receptors
scavenger receptors
2 ways to kill
oxygen dependent- respiratory burst. coupling of phagocytosis w/ ROS w/in lysosme. stimuli induce cytosolic proteins to localize to lysosome membrane to produce ROS
oxygen independent- lysozymes
important respiratory burst enzymes
NADPH oxidase multicomponent oxidase phagocyte oxidase- creates superoxide and H2O2 nitric oxide synthase- creates peroxynitrite
collateral damage of inflammation
4 types
normal- appropriate rxn against difficult to eradicate pathogens
autoimmunity- inappropriate defense rxn against host tissue
allergy- excessive defense rxn against harmless environmental substances
toxic- prolonged exposure to nondegradable exogenous material or endogenous toxi agents
most important damaging substances: lysozyme, ROS, NO
LAD1/2
recurrent infections d/t defective adhesion molecules
chronic granulomatous
organisms are ingested but not killed b/c of a lack of phacocyte oxidase
chediak-higashi syndrome
defective fusion of phasomes and lysosomes
inflammation terminatoin
passive and active
passive- neutrophils are short lived
mediators are short lived
active
- AA metabolites switch from pre to anti inflammatory lipoxins
- macrophages produced anti inflammatory cytokines
- anti-inflammatory lipid mediators
- neural impulses inhibit macrophage derived TNF
what mediators push macrophages towards M1 or M2
TLR ligands/ IFN-y - M1
IL13, 4- M2
scarring
connective tissue replacement
results after substantial tissue destruction and tissue paranchema cannot regenerate
chronic inflammation
prolonged duration in which tissue injury and attempts at repair coexist in varying combination
characterized by lymphocyte, plasma cell, and macrophages infiltrates
tissue destruction, angiogenesis, fibrosis
causes of chronic inflammation
persistent infections
immune mediated inflammatory disease
prolonged exposure to toxic agents
dominant player in chronic inflammation
macrophages
granuloma
an attempt by macrophages to “wall off” a difficult to destroy infectious agent
have giant cell and collar of lymphocytes