List the differences between endo vs. exotoxins
Describe the endotoxin LPS and the process by which it causes endotoxic shock
LPS - Lipopolysaccharide
coats the surface of Gram-negative bacteria (Lipid A - toxic component)
binding of LPS-TLR4 to receptor TLR4
-> varies responses (pro-inflammatory, endotoxic shock e. g. sepsis)
Describe how exotoxins are classified
classified in terms of specific target cell or site affected
enterotoxins: intestinal tract
neurotoxins: nervous system
leukocidins: innate and adaptive immune cells
haemolysins: disrupting the cell membrane of red blood cells
List the mechanisms by which exotoxins are toxic to host cells
inhibiting protein synthesis (C. diphteriae)
activating second messenger pathways (B. anthracis, V. cholerae)
activating immune responses (S. aureus superantigens)
damaging cell membranes (E. coli)
metalloprotease activity (C. tetani)
Provide examples of exotoxins (and their mode-of-action) produced by
V. cholerae
S. aureus
C. diphtheriae
UPEC (E. coli)
C. tetani
Name
mode of action
exotoxin produced
short circuit the immune system, triggering uncontrolled production of inflammatory mediators leading to a lethal cytokine strom
Staphylococcal enterotoxin B
crash critical cellular functions through transport of the toxic A-subunit into cells via phagocytosis -> electrolyte imbalance due to rapid efflux of Cl- ions by CFTR with decresed influx of N+ ions
Cholerae toxin (CTX/CT)
binding to toxin receptor on host cell membrane -> entering host via endocytosis -> release of catalytic A subunit -> prevention of ribosomal protein synthesis, subsequentialy causing cell death
Diphtheria toxin (DT)
UPEC
recruited by host membrane by protein receptors and/or specific interactions w. lipids -> concentration of toxins and start oligomerisation -> transmembrane pore forming -> promoting influx/efflux -> apoptosis/host cell death
pore forming toxin alpha hemolysin
inital binding at presynaptic terminals of neuromuscular junctions -> transportted to spinal cord -> motor neurons presynaptic terminals there -> destruction of VAMP -> inactivation of inhibitory neurotransmission -> enhanced excitability and activation of affected motor neurons
Tetanus toxin TeNT
Provide a general definition of a bacterial toxin
biologic virulence factors that prepare the host for colonisation
-> triggering a destructive process
-> function as autonomous molecular devices
-> targeting specific cells, punching holes in their membrane and/or modifying intracellular components
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