PMID- 10030794
OWN - NLM
STAT- MEDLINE
DCOM- 19990428
LR  - 20190915
IS  - 1073-2322 (Print)
IS  - 1073-2322 (Linking)
VI  - 11
IP  - 2
DP  - 1999 Feb
TI  - Role of tumor necrosis factor and interferon gamma in endotoxin-induced 
      E-selectin expression.
PG  - 93-7
AB  - Tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), potent 
      inflammatory cytokines, are released by macrophages during endotoxin shock. 
      However, the contribution of these cytokines to endotoxin-induced inflammation 
      has not been defined. The expression of E-selectin, measured using the dual 
      radiolabeled monoclonal antibody (mAb) technique, was monitored in different 
      tissues of endotoxin-challenged wild-type and IFN-gamma-deficient mice receiving 
      a mAb to TNF-alpha (TN3). A significant elevation in E-selectin expression 
      occurred in all tissues of wild-type mice challenged with endotoxin. Injection of 
      TN3 in wild-type mice significantly attenuated the endotoxin-induced 
      up-regulation of E-selectin in all tissues (p < .05) except the pancreas. The 
      level of reduction in endotoxin-induced E-selectin expression ranged between 30% 
      in the stomach to 60% in the small intestine. E-selectin expression in 
      endotoxin-challenged, IFN-gamma-deficient mice was significantly reduced in the 
      small and large intestines, when compared with endotoxin-challenged wild-type 
      mice. Although IFN-gamma deficiency had no effect on E-selectin expression in 
      other tissues, administration of TN3 to endotoxin-challenged, IFN-gamma-deficient 
      mice significantly reduced E-selectin expression to levels observed in 
      endotoxin-challenged, wild-type mice that received TN3. These findings indicate 
      that TNF-alpha is essential for achievement of maximal E-selectin expression in 
      most vascular beds during endotoxemia, whereas the contribution of IFN-gamma is 
      largely confined to the small intestine.
FAU - Eppihimer, M J
AU  - Eppihimer MJ
AD  - Department of Molecular and Cellular Physiology, Louisiana State University 
      Medical Center, Shreveport 71130, USA.
FAU - Russell, J
AU  - Russell J
FAU - Langley, R
AU  - Langley R
FAU - Gerritsen, M
AU  - Gerritsen M
FAU - Granger, D N
AU  - Granger DN
LA  - eng
GR  - P01 DK43785/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (E-Selectin)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/metabolism/pharmacology
MH  - E-Selectin/drug effects/*metabolism
MH  - Endothelium, Vascular/metabolism
MH  - Escherichia coli
MH  - Gastric Mucosa/metabolism
MH  - Interferon-gamma/genetics/*metabolism
MH  - Intestine, Large/metabolism
MH  - Intestine, Small/metabolism
MH  - Lipopolysaccharides
MH  - Lung/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Mutant Strains
MH  - Organ Specificity
MH  - Shock, Septic/chemically induced/*metabolism
MH  - Tumor Necrosis Factor-alpha/*metabolism
EDAT- 1999/02/25 00:00
MHDA- 1999/02/25 00:01
CRDT- 1999/02/25 00:00
PHST- 1999/02/25 00:00 [pubmed]
PHST- 1999/02/25 00:01 [medline]
PHST- 1999/02/25 00:00 [entrez]
AID - 10.1097/00024382-199902000-00004 [doi]
PST - ppublish
SO  - Shock. 1999 Feb;11(2):93-7. doi: 10.1097/00024382-199902000-00004.