NECROSIS FWTOR-&CRCHECTIN OF HUTWN NEUTROPHILS PHOSPHOINOSITIDES MD
Carlo
LCIUDTWNR,
Institute
of
Received
November
GWTIWTES INDEPENDENTLY THE RELECISE OF
#IRON,
Shmuel
Giorgio
Pathology,
General
29,
AND BIOPHYSICAL RESEARCH COMMUNICATIONS Pages 308-315
THE Oe--GENERQTING OF THE HYDROLYSIS
fiRCICHIDONIC
BERTON
University
Filippo
and
of
OF
CICID ROSS1
Verona,
Verona,
Italy
1989
have investigated the mechanisms of transnenbrane implicated in the activation of the respiratory burst of adherent neutrophils by tumor necrosis factor-n/cachectin (TNF) . The activation of the respiratory burst by TNF is insensitive to pertussis toxin and weakly sensitive to protein kinase C inhibitors Cytochalasin I3 and dibutyryl cyclic RhP have an inhibitory effect. The activation of the respiratory burst by TNF takes place in the absence of formation of =H-inositol phosphates, 32P-phosphatidic acid, and =H-arachidonic acid. These results demonstrate that the activation of the respiratory burst by an endogenous, physiologic stimulus can be independent of the formation of messengers derived from hydrolysis of phosphoinositides. 0 1990 Academic Press, Inc. SUIIHRRY,
Ue
signalling
Tumor
necrosis
cytokine
factor-w
able
inflammatory (1).
to
modulate
reactions, is
TNF
neutrophils 1s
a
and
ion
TNF
was
a
molecules to
proteins,
they
NRDPH
of
of
(reviewed
in
activate
NRDPH
0006-291x/90 Copyright All rights
amounts
signals
oxidase
that
is ligand-receptor
are
accompanied
$1.50
0 1990 by Academic Press, Inc. of reproduction in any form reserved.
cachectin activates the O2(-)-generating system of human neutrophils independently of the hydrolysis of phosphoinositides and the release of arachidonic acid.
We have investigated the mechanisms of transmembrane signalling implicated in the activation of the respiratory burst of adherent neutrophils by tumor...