Possible association of granulocyte mobilization to the peritoneal cavity with ZnCl2-induced protection against endotoxin.
We have attempted to determine which components of the inflammatory response are responsible for ZnCl2-induced retention of endotoxin in the peritoneal cavity and enhancement of survival following challange with the toxin. ZnCl2 injected intraperitoneally into mice caused accumulation of granulocytes in the peritoneal cavity, but these cells were apparently not responsible for the trapping process. This contention in supported by our observation that reduction of hepatosplenic uptake of 51CR-labeled endotonxin was similar in unirradiated mice and in mice made by irradiation (1000 rad 60 Co) 1 rad = 10 (-2) J/kg). Hepatosplenic uptake was also depressed when untreated mice were injected with endotoxin suspended in cell-free plasma. Furthermore, zinc did not protect irradiated mice challanged with endotoxin, although it enhanced survival in urirradiated animals. Lack of protection in irradiated mice may be due to a deficiency in the cellular response in the peritoneal cavity.
D000818:Animals; D001202:Ascitic Fluid / Q000166:cytology; D002465:Cell Movement / Q000187:drug effects; D004731:Endotoxins / Q000037:antagonists & inhibitors* / Q000633:toxicity; D006098:Granulocytes / Q000187:drug effects / Q000502:physiology*; D007274:Injections, Intraperitoneal; D007962:Leukocytes / Q000502:physiology*; D008297:Male; D051379:Mice; D012485:Salmonella typhi; D015032:Zinc / Q000494:pharmacology*
D004731:Endotoxins; D015032:Zinc