Role of phospholipase-associated penetration mechanism in cell injury by Rickettsia rickettsii.
The cholesterol receptor-binding drugs amphotericin B and digitonin reduced rickettsial plaque formation, presumably by blocking rickettsial attachment, even when added to the plaque model on day 4 post-inoculation when infected foci were well established. The phospholipase inhibitor phentermine reduced plaque formation, presumably by inhibiting the phospholipase-associated entry step of penetration.
D000666:Amphotericin B / Q000494:pharmacology; D000818:Animals; D002462:Cell Membrane / Q000502:physiology; D002478:Cells, Cultured; D002642:Chick Embryo; D002784:Cholesterol / Q000378:metabolism; D004072:Digitonin / Q000494:pharmacology; D010645:Phentermine / Q000494:pharmacology; D010740:Phospholipases / Q000037:antagonists & inhibitors; D012284:Rickettsia rickettsii / Q000472:pathogenicity*; D012373:Rocky Mountain Spotted Fever / Q000382:microbiology*
D000666:Amphotericin B; D002784:Cholesterol; D010645:Phentermine; D010740:Phospholipases; D004072:Digitonin