innate immune protection Flashcards
how is the skin an effective physical barrier
produces anti-microbial compounds eg psoriasin
how is the respiratory tract an effective physical barrier
tight junctions-> pathogens cant go between
cilia-> sweeps pathogens away
mucous
how is the GI tract an effective physical barrier
peristalsis
low pH
how do eyes keep pathogens out?
blinking
tears (contain lysozymes)
how does the body recognise pathogens?
highly conserved molecular structures called PAMPS (pathogen associated molecular patterns) which are critical to the survival of pathogen
not present in host
PAMPs in gram negative and gram positive bacteria
gram negative: lipidA
gram positive: lipotechoic acid
what is the name of the receptor that recognISES pamps? What are the three types of this receptor
PRR (pattern recognition receptor)
- collectin (in serum)
- toll-like receptor (on cm)
- nod like receptor (in cytoplasm)
structure of collectin, where is it found
in serum
consists of
collagen-like region (interacts with effector parts of immune system)
lectin region (has mannose-binding lectin that binds to sugar molecules on surface of pathogen of a particular arrangement)
toll-like receptors types what do they bind to
many types
bind to LPS on gram -ve; peptidoglycan on gram +ve
unmethylated DNA (human dna is largely methylated)
ssRNA/ssDNA of viruses
flagellin
NOD like receptors types and mechanism; what does it stand for
nuclear oligomerisation domain receptor;
type 1 and 2
senses PAMPS-> sends signal to nu -> nu upregulates immune response-> increased chemokines and cytokines
what are complements? how do they operate? what do they result in? what triggers their synthesis and where?
inflammation triggers synthesis in liver
series of proteins
operate in cascade
C3 convertase converts C3 into C3a and b
C3a binds to C3a receptors on macrophages and neutrophils-> recruitment to inflammation site
C3b -> opsinisation
C3 activates terminal components-> assemble and form membrane attack complex-> insert into pathogen cm-> osmotic potential of pathogen disrupted
which wbcs undergo phagocytosis? what are their characteristics?
monocyte (in blood)-> macrophage (in tissues): found in lungs/liver/GI tract, long lived
neutrophils: only present in blood and pus, short lived
steps in phagocytosis
chemotaxi-> pseudoposia extrudes from phagocyte-> PAMP on pathogen recognised by PRR -> engulf-> phagosome with low pH-> lysosome fusion-> phagolysosome-> digestion-> residual body removed/antigens displayed on cell surface-> T cell activation
phagocyte killing mechanism involving ROS
(more so for neutrolphils) following phagocytosis-> increase in o2 uptake-> NADPH complex assembles on phagosome membrane-> oxygen reduced by NADPH oxidase to form hydroxyl radicals + hypochlorite-> DNA damage and damage to bacterial membranes
phagocyte killing mechanism involving reactive nitrogen intermediates
(more so for macrophages)
binding of bacterial components/interferon gamma/tumour necrosis factor to phagocyte-> NO synthetase upregulated-> o2 + L-arg-> NO + citrulline-> DNA damage and damage to bact membranes
