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LPS induces Caspase-1 NLRP3 Pyroptosome
Lipopolysaccharide Induces Caspases-1 NLRP3 Pyroptosome
Pathway
Spencer E. Thomas !rancesca ". #er$ic %illiam N. &erd
Department of Biomedical Science, Missouri State University,
Springfield MO 6589
!"unning title# $%S induces &aspase'( )$"%* %yroptosome
+ddress correspondence to# Spencer , -.omas, Department of
Biomedical Science, Missouri StateUniversity, Springfield MO 6589/
'mail# set0561live/missouristateuniversity/edu
'eywords( &aspase'(, )od'li2e receptor 3)$"4, )$"%*,
%yroptosis,
)ac*+round( -.e role of liposacc.aride 3$%S4,
)$"% inflammasome, and caspase'( may involve
)$"%* independent pat.ays/
Results( In vitro analysis of Casp-1-/- BMDM
demonstrated pyroptotic cell deat. in response to
$%S not only reuires +-% 7ut is mediated 7y
caspase'( it. pyroptotic cell deat., post'$%Sc.allenge, o7served
to 7e (6/6 */(8 and56/5 /:8 in ;- and Casp-1-/- BMDMs,
respectively/ ;estern 7lot findings ere
inconclusive, it. no significant c.anges in pro'
t.us no )$"%* inflammasome
activation/
Conclusion(-.e e?act roles of t.e )$"%* andcaspase'( in
pro'inflammatory 3
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LPS induces Caspase-1 NLRP3 Pyroptosome
of purported to 7e
mediated 7y caspase'( and caspase'((, respect'ively/
&ontroversy surrounding t.e role of t.e
)$"%* pyroptosome in t.e non'canonical
caspase'(( pat.ay suggests differential cyto2ine
signaling patterns, specifically .ic. reuires caspase'(
dependent activation 7y
)$"%* 3((, (0, (54/
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LPS induces Caspase-1 NLRP3 Pyroptosome
control samples 3+-%'4 ere diluted it. eual
volume of deionied NO> e?perimental samplesere conducted in
duplicate/
"lo# Cytometry!Hlo cytometry analysis
as performed folloing $%S c.allenge to
determine level of cytoto?icity 3pyroptosis4 as
previously descri7ed 3(4/
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LPS induces Caspase-1 NLRP3 Pyroptosome
t.e ensuing proteolytic activation of caspase'((
3:4/ Similar researc. .as led to t.e adoption of t.e
t.eory t.at cytosolic $%S induced caspase'((
activation .ic. may facilitate t.e 7ioactive
caspase'( conformation/ Noever, contemporaryfindings of t.e
e?tracellular and intracellular
presence of s.o t.at )$"%* pyroptosomeactivation of caspase'(
may antagonie caspase'
((, and vice'versa 3*, (*4/ +n alternate .ypot.esis
for t.e current findings is t.at insufficient
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!I2RE 1. LPS induced NLRP pyroptosis is dependent on caspase-1.
Hlo cytometry analysis
as conducted on %
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!I2RE 3. Casp-1-/-does not decrease pro-IL-14 or IL-14 in vitro.
%rotein density of pro'
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RE!ERENCES
(/ Bru7a2er, S/ ;/, Bon.am, K/ S/, Vanoni,
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signaling and +D%'evo2ed platelet aggregation/
.ol( Pharmacol(79, :0*F:5(
(9/ "ivers'+uty, /, and Broug., D/ 3:(54
%otassium efflu? fires t.e canon# %otassium
efflu? as a common trigger for canonical and
noncanonical )$"%* pat.ays/+ur( (
Immunol(65, :58F:6(
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