TY - JOUR
T1 - Circulating interleukin-1 and tumor necrosis factor in septic shock and experimental endotoxin fever
AU - Cannon, Joseph Gerard
AU - Tompkins, Ronald G.
AU - Gelfand, Jeffrey A.
AU - Michie, Hamish R.
AU - Stanford, Gregory G.
AU - van der Meer, Jos W.M.
AU - Endres, Stefan
AU - Lonnemann, Gerhard
AU - Corsetti, John
AU - Chernow, Bart
AU - Wilmore, Douglas W.
AU - Wolff, Sheldon M.
AU - Burke, John F.
AU - Dinarello, Charles A.
N1 - Funding Information:
Supportedbygrants GM-21700and GM-07035 (National Instituteof General Medical Sciences), AI-15614 (National Institute of Allergy and Infectious Diseases), and AR-39595 (National Institute of Arthritis and Musculoskeletal and Skin Diseases) and by the Louviers Foundation.
PY - 1990/1
Y1 - 1990/1
N2 - Interleukins (IL)-1β and -1α and tumor necrosis factor (TNF-α) were measured by radioimmunoassay in plasma samples from 44 healthy individuals, 15 patients in septic shock, and 6 volunteers infused with endotoxin. Plasma IL-1α levels were low (40 pg/ml) or undetectable in all situations. In 67% ofthe healthy subjects, plasma IL-1β levels were <70 pg/ml. Septic patients had higher plasma IL-1β levels (120± 17pg/ml, P =.001);those of surviving patients were higher than those of patients who died (P =.05). Plasma TNF-α concentrations in septic individuals were elevated (119 ± 30 pg/ml) and correlated with severity of illness (r =.73, P =.003), but no correlation was observed between plasma IL-1β and TNF-α concentrations in individual samples. Infusion of endotoxin caused a twofold elevation of IL-1β, from a baseline of 35 ± 5 pg/ml to a maximum of 69 ± 27 pg/ml at 180min (P<.05). Peak TNF-α levels after endotoxin infusion were 15 times higher than IL-1β levels, were attained more rapidly (90 min), and as with the septic patients, did not correlate with IL-1β levels. These data support the concept that plasma IL-1β and TNF-α concentrations are regulated independently and are associated with different clinical outcomes.
AB - Interleukins (IL)-1β and -1α and tumor necrosis factor (TNF-α) were measured by radioimmunoassay in plasma samples from 44 healthy individuals, 15 patients in septic shock, and 6 volunteers infused with endotoxin. Plasma IL-1α levels were low (40 pg/ml) or undetectable in all situations. In 67% ofthe healthy subjects, plasma IL-1β levels were <70 pg/ml. Septic patients had higher plasma IL-1β levels (120± 17pg/ml, P =.001);those of surviving patients were higher than those of patients who died (P =.05). Plasma TNF-α concentrations in septic individuals were elevated (119 ± 30 pg/ml) and correlated with severity of illness (r =.73, P =.003), but no correlation was observed between plasma IL-1β and TNF-α concentrations in individual samples. Infusion of endotoxin caused a twofold elevation of IL-1β, from a baseline of 35 ± 5 pg/ml to a maximum of 69 ± 27 pg/ml at 180min (P<.05). Peak TNF-α levels after endotoxin infusion were 15 times higher than IL-1β levels, were attained more rapidly (90 min), and as with the septic patients, did not correlate with IL-1β levels. These data support the concept that plasma IL-1β and TNF-α concentrations are regulated independently and are associated with different clinical outcomes.
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U2 - 10.1093/infdis/161.1.79
DO - 10.1093/infdis/161.1.79
M3 - Article
C2 - 2295861
AN - SCOPUS:0025017232
SN - 0022-1899
VL - 161
SP - 79
EP - 84
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 1
ER -