PMID- 7806369
OWN - NLM
STAT- MEDLINE
DCOM- 19950202
LR  - 20210526
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 63
IP  - 1
DP  - 1995 Jan
TI  - Tumor necrosis factor (TNF)-dependent shedding of the p55 TNF receptor in a 
      baboon model of bacteremia.
PG  - 297-300
AB  - We have tested the hypothesis that the tumor necrosis factor (TNF) plays a 
      significant role in vivo in TNF receptor shedding and studied the release of 
      TNF-binding protein 1 (TNF-BP1), the soluble fragment of the 55- to 60-kDa TNF 
      alpha (TNF) receptor, in a baboon model of Escherichia coli bacteremia, using 
      three different doses of bacteria in acute infection (8 h) experiments (n 
      [animals] = 11) and a single dose in a subchronic infection (72 h) experiment. In 
      the subchronic infection study, one group of animals (n = 6) was pretreated with 
      a neutralizing murine monoclonal antibody to TNF (CB0006). Concentrations of TNF 
      and TNF-BP1 in plasma were determined in specific, monoclonal antibody-based 
      immunoassays. Untreated animals (n = 6) showed undetectable TNF concentrations (< 
      10 pg/ml at baseline), whereas TNF-BP1 levels in plasma were in the range of 2 
      ng/ml, similar to concentrations observed in humans. Infusion of bacteria 
      resulted in a rapid, dose-dependent increase in plasma TNF concentrations that 
      reached a maximal level after 2 h and returned to baseline within 6 h. TNF-BP1 
      concentrations also showed a dose-dependent increase to peak concentrations 
      three- to fivefold above baseline within 2 h but, in contrast to TNF levels, 
      remained significantly elevated for up to 48 h. In animals pretreated with 
      antibody CB0006, circulating TNF was completely neutralized, and TNF-BP1 was 
      significantly reduced. We conclude that TNF-BP1 is released in bacteremia and 
      that release in vivo is partially dependent on the presence of TNF.
FAU - Redl, H
AU  - Redl H
AD  - Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, 
      Austria.
FAU - Schlag, G
AU  - Schlag G
FAU - Adolf, G R
AU  - Adolf GR
FAU - Natmessnig, B
AU  - Natmessnig B
FAU - Davies, J
AU  - Davies J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Antigens, CD)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - *Antigens, CD
MH  - Bacteremia/*metabolism
MH  - Chronic Disease
MH  - Disease Models, Animal
MH  - Escherichia coli Infections/*metabolism
MH  - Male
MH  - Neutralization Tests
MH  - Papio
MH  - Receptors, Tumor Necrosis Factor/*metabolism
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Shock, Septic/*metabolism
MH  - Tumor Necrosis Factor-alpha/immunology/*metabolism
PMC - PMC172991
EDAT- 1995/01/01 00:00
MHDA- 1995/01/01 00:01
PMCR- 1995/01/01
CRDT- 1995/01/01 00:00
PHST- 1995/01/01 00:00 [pubmed]
PHST- 1995/01/01 00:01 [medline]
PHST- 1995/01/01 00:00 [entrez]
PHST- 1995/01/01 00:00 [pmc-release]
AID - 10.1128/iai.63.1.297-300.1995 [doi]
PST - ppublish
SO  - Infect Immun. 1995 Jan;63(1):297-300. doi: 10.1128/iai.63.1.297-300.1995.