Enhanced release of TNF-alpha, but not IL-1 beta, from uremic blood after endotoxin stimulation.
Aberrant immunologic host defenses associated with uremia may be a cause of the high incidence of sepsis in chronic hemodialysis (CHD) patients. This investigation determined the cytokine response of blood from five nondialyzed chronic renal failure (CRF) patients, five CHD patients, and five healthy controls (HC) after in vitro stimulation with 1 ng/ml Escherichia coli 0113 endotoxin. Concentrations of the cytokines TNF-alpha and IL-1 beta were determined by ELISA and were similar in all baseline and unspiked samples. TNF-alpha concentrations in CRF and CHD spiked samples were similar to each other but significantly greater (p less than 0.01) than in HC spiked samples. IL-1 beta concentrations in CRF, CHD, and HC-spiked samples were not significantly different. We conclude that CRF and CHD patients have enhanced TNF-alpha response, which may be related to uremia and not dialysis-related factors. Uremia does not potentiate IL-1 beta release.
Powell
A C
AC
Department of Medicine, Emory University School of Medicine, Atlanta, GA.
Bland
L A
LA
Oettinger
C W
CW
McAllister
S K
SK
Oliver
J C
JC
Arduino
M J
MJ
Favero
M S
MS
D002482:Cellulose / Q000031:analogs & derivatives / Q000494:pharmacology; D004731:Endotoxins / Q000494:pharmacology; D004926:Escherichia coli; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000097:blood*; D007676:Kidney Failure, Chronic / Q000097:blood*; D008297:Male; D006435:Renal Dialysis; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis*; D014511:Uremia / Q000097:blood*
D004731:Endotoxins; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D002482:Cellulose; C009865:cuprammonium cellulose