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(Received for publication, March 29, 1995; and in revised form, July 9,
1995) This study demonstrates that lipopolysaccharide (LPS) mediates
induction of transcription factor NF
Volume 270,
Number 43,
Issue of October 27, 1995 pp. 25418-25425
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
B and activation of the
cytomegalovirus (CMV) promoter-enhancer in the SW480 cell line. These
cells do not express a functional membrane CD14. The LPS response in
SW480 cells was weaker and markedly slower than the tumor necrosis
factor (TNF) response. Pretreatment with TNF for 72 h inhibited both
TNF, tumor necrosis factor receptor (TNFR) p55, TNFR p75, and
LPS-mediated activation of nuclear factor -
B (NF
B), whereas
pretreatment with LPS only inhibited the LPS response. TNFR p55
antibody pretreatment resulted in marked inhibition of the LPS
response, while pretreatment with TNFR p75 antiserum only had a weak
inhibitory effect. Flowcytometric analysis showed that LPS binding as
well as expression of TNFR p55 and TNFR p75 were not affected by LPS or
TNF pretreatment, indicating that the observed inhibition is not due to
reduction of specific binding sites at the cell surface. The results
suggest that LPS signaling in SW480 cells involves intracellular
components which may be depleted or inactivated via TNFR p55,
indicating that the LPS and TNFR p55 pathways overlap. We propose that
TNFR p55 can mediate activation of NF
B and cytomegalovirus
promoter-enhancer in SW480 cells via two distinct mechanisms, one which
is activated only via TNFR p55 and leads to rapid activation of
NF
B, and another which is overlapping with the LPS pathway.
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