Lecture 14 - Listeria Flashcards
Phyla?
Firmicutes
Route of transmission
Feco-oral route
Disease
Listeriosis
Motility?
Outside of host - Peritrichous flagella
Inside cell - Actin nucleation (theft)
How pathogenic is it?
20-30% mortality rate
Flu like symptoms in healthy individuals (stomach bug)
Dangerous in older/immunocompromised/pregnant women
Why is it hard to trace the source of outbreak?
11-70 days incubation time
How does Lm infection progress in host?
Enters via feco-oral route, crosses intestinal barrier and reproduces in liver and spleen, in immunocompromised individuals goes on to cause bacteremia, then septic shock or spread to brain (meningitis) or placenta (abortion)
What kinds of cells can they infect?
Epithelial, endothelial, neurons, hepatocytes, phagocytic cells
What does InA bind to on host cell? How does it bind? On what cells?
E-Cadherin. Ectodomain binds to E-cadherin, which recruits other E-cadherins on host cell membrane, leading to autophosphorylation and ubiquitination, recruiting clathrin and actin leading to endocytosis. Intestinal epithelial cells.
What does InB bind to on host cell? How does it bind? On what cells?
Met. Ectodomain binds to Met, which recruits other Met leading to dimerization, leading to autophosphorylation and ubiquitination, recruiting clathrin and actin leading to endocytosis. Broad specificity - many cell types.
How does LLO lyse vacuoles in infected cells? How does Lm make sure the host cell isn’t lysed after escape from vacuole?
Listeria releases soluble LLO, binds to host membrane in cholesterol dependent manner, insertion of TMH1 and TMH2. Adjacent LLOs form the pore. LLO is only active in low pH environment
How does Lm use PlcA and PlcB to lyse double-vacuoles? How do double vacuoles arise? Why are these important when Lm already has LLO?
Secreted enzymes that degrade phospholipids- cleave phosphodiester bond between phosphate and glycerol in the polar head group. During transcytosis. Because sometimes vacuoles do not undergo pH reduction.
How does Lm “steal” actin?
Lm subverts host actin nucleation machinery (WASP) to polymerize actin on one end in order to propel itself in the cytoplasm. Actin monomers from the cell are stolen to polymerize chain off which to push off.
How do InA/B get recognized by host cell receptors if they are viral receptors?
Because they mimic host cell TLR4 via LRRs
How are InA/B bound to the bacteria?
InA is covalently attached to the peptidoglycan cell wall and InB is attached to LTA which is bound to the membrane.
