PMID- 1425922
OWN - NLM
STAT- MEDLINE
DCOM- 19921208
LR  - 20141120
IS  - 0014-2980 (Print)
IS  - 0014-2980 (Linking)
VI  - 22
IP  - 11
DP  - 1992 Nov
TI  - Heat shock prevents lipopolysaccharide-induced tumor necrosis factor-alpha 
      synthesis by rat mononuclear phagocytes.
PG  - 2983-7
AB  - Tumor necrosis factor-alpha (TNF-alpha), a mononuclear phagocyte-derived peptide 
      is known to participate in the pathogenesis of fever. To determine whether a 
      feedback mechanism exists by which elevated temperatures influence TNF-alpha 
      generation, we have examined the effects of heat shock on the in vitro synthesis 
      of TNF-alpha by rat glomeruli, inflammatory peritoneal macrophages and blood 
      monocytes. Preexposure of peritoneal macrophages to elevated temperatures for 20 
      min decreased the subsequent lipopolysaccharide-induced release of TNF-alpha 
      bioactivity. The mean reductions were 11.9 +/- 5.0%, 86.3 +/- 12.0%, and 95.2 +/- 
      3.5% after pretreatment at 39, 41 and 43 degrees C, respectively. Reductions, 
      that were transient, were maximum when lipopolysaccharide was added 0-2 h after 
      heat shock. They correlated with the decreased release of immunoreactive 
      TNF-alpha and the decreased expression of both cell-associated TNF-alpha molecule 
      and TNF-alpha mRNA. Heat shock-induced inhibition of TNF-alpha release was 
      independent of variations of prostaglandin synthesis, but was possibly related to 
      the induction of heat-shock proteins since (a) macrophages exposed to heat shock 
      synthesized the major 70- and 90-kDa heat-shock proteins, and (b) chemical 
      inducers of the heat-shock response were also effective inhibitors of TNF-alpha 
      release. The mean reduction of TNF-alpha release after pretreatment at 41 degrees 
      C was found to be identical in glomerular tissue (82.0 +/- 7.5%), but 
      significantly less in blood monocytes (43.9 +/- 10.9%). This supports the 
      hypothesis that a negative-feedback mechanism exists between elevated temperature 
      and lipopolysaccharide-induced TNF-alpha synthesis, and suggests that this 
      regulation is less active in blood monocytes than in tissue macrophages.
FAU - Fouqueray, B
AU  - Fouqueray B
AD  - INSERM U. 64, Hopital Tenon, Paris, France.
FAU - Philippe, C
AU  - Philippe C
FAU - Amrani, A
AU  - Amrani A
FAU - Perez, J
AU  - Perez J
FAU - Baud, L
AU  - Baud L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Eur J Immunol
JT  - European journal of immunology
JID - 1273201
RN  - 0 (Heat-Shock Proteins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Heat-Shock Proteins/biosynthesis
MH  - *Hot Temperature
MH  - In Vitro Techniques
MH  - *Lipopolysaccharides
MH  - Macrophages/drug effects/*metabolism
MH  - Male
MH  - Monocytes/drug effects/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
EDAT- 1992/11/01 00:00
MHDA- 1992/11/01 00:01
CRDT- 1992/11/01 00:00
PHST- 1992/11/01 00:00 [pubmed]
PHST- 1992/11/01 00:01 [medline]
PHST- 1992/11/01 00:00 [entrez]
AID - 10.1002/eji.1830221133 [doi]
PST - ppublish
SO  - Eur J Immunol. 1992 Nov;22(11):2983-7. doi: 10.1002/eji.1830221133.