Clostridium perfringens epsilon toxin induces blood brain barrier permeability via caveolae-dependent transcytosis and requires expression of MAL
Fig 3
Epsilon toxin does not bind to the microvasculature of other peripheral organs.
Wild type mice expressing Mal+/+ or mice deficient in Mal-/- were intravenously injected ETX-594 for ten minutes then perfused with PBS to remove unbound toxin. ETX binding to microvasculature was evaluated in tissue cyrosections. FITC-BSL1 was used to visualize microvasculature. ETX bound to the epithelial cells of renal tubules of Mal+/+ mice (white arrows) but not the glomerular capillaries (asterisks). In Mal-/- mice, ETX, can be seen accumulating in unidentified renal structures (white arrow heads). ETX is also observed binding to the microvasculature of the intestines in Mal+/+ mice (white arrows), but not Mal-/- mice. ETX binding was not observed in the spleen, lung, liver or heart of Mal+/+ or Mal-/- animals.