A role for hemolysin in Escherichia coli-induced inflammation in granulocytopenic rabbits.
Inflammation induced in the skin of granulocytopenic rabbits by Escherichia coli was examined. Protein exudation and platelet deposition in lesions were measured with 125I-labeled albumin and 111In-labeled platelets. In granulocytopenic rabbits 10(4)-10(7) live serum-resistant E. coli induced protein exudation and platelet deposition beginning at 3 hr and then progressing over the next 24 hr to much higher levels than in normal rabbits. These responses were associated with interstitial edema and progressive venous thrombosis in the absence of leukocytes; no such reactions were observed in normal rabbits. No reactions were induced in granulocytopenic rabbits by killed E. coli. Of six E. coli strains tested, all three hemolytic strains induced lesions with four to five times more thrombosis (platelet deposition) than did nonhemolytic strains. Two hemolysin-negative mutants lost most of their thrombogenic activity. All three hemolytic strains had cell-associated hemolysin, but only one of these elaborated appreciable free, filterable hemolysin as well.
D000380:Agranulocytosis / Q000150:complications*; D000818:Animals; D001792:Blood Platelets / Q000166:cytology; D002199:Capillary Permeability; D004927:Escherichia coli Infections / Q000473:pathology*; D005260:Female; D006460:Hemolysin Proteins / Q000502:physiology*; D007249:Inflammation / Q000382:microbiology / Q000473:pathology*; D008297:Male; D008466:Mechlorethamine; D011817:Rabbits; D013997:Time Factors
D006460:Hemolysin Proteins; D008466:Mechlorethamine