PMID- 10455905
OWN - NLM
STAT- MEDLINE
DCOM- 19990902
LR  - 20071114
IS  - 0039-6060 (Print)
IS  - 0039-6060 (Linking)
VI  - 126
IP  - 2
DP  - 1999 Aug
TI  - Discordant tumor necrosis factor-alpha superfamily gene expression in bacterial 
      peritonitis and endotoxemic shock.
PG  - 349-57
AB  - BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) is a member of a large family 
      of predominantly homotrimeric type II membrane-associated proteins with both 
      proinflammatory and apoptosis-inducing properties. Although TNF-alpha expression 
      has been studied extensively, little is known about the expression of other 
      members of the TNF-alpha superfamily during acute inflammatory processes. 
      METHODS: TNF-alpha, Fas ligand (FasL), and TRAIL (tumor necrosis factor-related 
      apoptosis-inducing ligand) messenger RNA (mRNA) expression were examined in 
      liver, lung, spleen, and kidney after either a cecal ligation and puncture or 
      endotoxemic shock with use of semiquantitative reverse transcriptase-polymerase 
      chain reaction. RESULTS: Cecal ligation and puncture increased TNF-alpha mRNA in 
      lung and liver (both P < .05) within 3 hours, which was paralleled by increased 
      FasL mRNA. In the spleen TNF-alpha and FasL mRNA significantly declined (both P < 
      .05). In contrast to TNF-alpha and FasL, TRAIL mRNA levels were unchanged in all 
      organs except lung, where it was reduced at 24 hours (P < .05). Endotoxemic shock 
      also increased lung TNF-alpha and FasL mRNA levels (both P < .05). CONCLUSIONS: 
      In acute inflammatory processes TNF-alpha and FasL mRNA increase concordantly in 
      several solid organs. In contrast, TRAIL mRNA levels do not consistently change 
      during these acute inflammatory processes, suggesting that its expression is 
      under independent and discordant regulatory control.
FAU - Tannahill, C L
AU  - Tannahill CL
AD  - Department of Surgery, University of Florida College of Medicine, Gainesville 
      32610-0286, USA.
FAU - Fukuzuka, K
AU  - Fukuzuka K
FAU - Marum, T
AU  - Marum T
FAU - Abouhamze, Z
AU  - Abouhamze Z
FAU - MacKay, S L
AU  - MacKay SL
FAU - Copeland, E M 3rd
AU  - Copeland EM 3rd
FAU - Moldawer, L L
AU  - Moldawer LL
LA  - eng
GR  - GM40586-11/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Surgery
JT  - Surgery
JID - 0417347
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (Fas Ligand Protein)
RN  - 0 (Fasl protein, mouse)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (TNF-Related Apoptosis-Inducing Ligand)
RN  - 0 (Tnfsf10 protein, mouse)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Apoptosis Regulatory Proteins
MH  - Bacterial Infections/*metabolism
MH  - Fas Ligand Protein
MH  - Female
MH  - Lipopolysaccharides/pharmacology
MH  - Membrane Glycoproteins/genetics
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Peritonitis/*metabolism
MH  - Polymerase Chain Reaction
MH  - RNA, Messenger/*analysis
MH  - Shock, Septic/*metabolism
MH  - TNF-Related Apoptosis-Inducing Ligand
MH  - Tumor Necrosis Factor-alpha/*genetics
EDAT- 1999/08/24 10:00
MHDA- 2001/03/28 10:01
CRDT- 1999/08/24 10:00
PHST- 1999/08/24 10:00 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1999/08/24 10:00 [entrez]
AID - S0039606099002093 [pii]
PST - ppublish
SO  - Surgery. 1999 Aug;126(2):349-57.