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1 eading to fever and inflammatory cell death (pyroptosis).
2 ns (IL)-1beta and 18 and elicits cell death (pyroptosis).
3 and the induction of rapid host cell death (pyroptosis).
4 8 as well as caspase 1-dependent cell death (pyroptosis).
5 plasma membrane to induce secondary necrosis/pyroptosis.
6 ronic inflammatory response generated during pyroptosis.
7 g mammalian cells when it is released during pyroptosis.
8 y pathogens have evolved to avoid or subvert pyroptosis.
9 ammasome assembly, caspase-1 activation, and pyroptosis.
10 eased from GSDMD acts as an effector in cell pyroptosis.
11 erovar Typhimurium reduced flagellin-induced pyroptosis.
12 ent agonists and act independently to induce pyroptosis.
13 aspase-1-mediated production of IL-1beta and pyroptosis.
14 ependent on ASC but independent of NLRP3 and pyroptosis.
15 of an inflammatory cell death pathway termed pyroptosis.
16 l blood-derived CD4 T cells naturally resist pyroptosis.
17 1beta causing inflammation and cell death by pyroptosis.
18 essential for ATP release and P2X7-mediated pyroptosis.
19 omerization to activate caspase-1 and induce pyroptosis.
20 form of lytic, programmed cell death called pyroptosis.
21 1beta (pro-IL-1beta) and pro-IL-18 and drive pyroptosis.
22 kin-18 and a lytic form of cell death termed pyroptosis.
23 s inflammatory cell death that is defined as pyroptosis.
24 nd an inflammatory form of cell death called pyroptosis.
25 urified from co-cultures lose sensitivity to pyroptosis.
26 esponse, leading to caspase-1 activation and pyroptosis.
27 on of human airway epithelia can also induce pyroptosis.
28 of presynthesized inflammatory molecules and pyroptosis.
29 nd obliteration of the replicative niche via pyroptosis.
30 atforms called inflammasomes is required for pyroptosis.
31 pase-1 to produce mature IL-1beta and induce pyroptosis.
32 to more recently discovered pathways such as pyroptosis.
33 on have lower microtubule stability and less pyroptosis.
34 pecific tubulin isoforms in the execution of pyroptosis.
35 L)-1beta and IL-18 secretion, and macrophage pyroptosis.
36 d induce the inflammatory form of cell death pyroptosis.
37 y cytokines, pro-IL-1beta and pro-IL-18, and pyroptosis.
38 d and inflammatory form of cell death termed pyroptosis.
39 d form of lytic programmed cell death termed pyroptosis.
40 of proinflammatory IL-1beta, consistent with pyroptosis.
41 poly(I:C)-treated uterus, which could induce pyroptosis.
42 n of interleukin 1beta (IL-1beta), IL-18 and pyroptosis.
43 duced IL-1 release occurred independently of pyroptosis.
44 mplex that promotes caspase-1 activation and pyroptosis.
45 and secretion of IL-1beta and IL-18 but not pyroptosis.
46 ta (IL-1beta) and IL-18 and the induction of pyroptosis.
47 -1beta (IL-1beta) and IL-18 and induction of pyroptosis.
48 novo protein synthesis before committing to pyroptosis.
49 orms membrane-disrupting pores, and executes pyroptosis.
50 ll as lytic inflammatory cell death known as pyroptosis.
51 ry cytokines and a form of cell death called pyroptosis.
52 ircumstances, the induction of cell death by pyroptosis.
53 and initiates a lytic host cell death called pyroptosis.
54 on of a special type of cell death, known as pyroptosis.
55 and both enhance the antimicrobial nature of pyroptosis.
56 and induces the proinflammatory cell death, pyroptosis.
57 ns, signifying the inflammatory potential of pyroptosis.
58 rophage cytosol, resulting in AIM2-dependent pyroptosis.
59 tokines interleukin (IL)-1beta and IL-18 and pyroptosis.
60 at robustly activate necrosis, apoptosis, or pyroptosis.
61 proteins that suppress apoptosis and promote pyroptosis.
62 that suppress apoptosis and thereby promote pyroptosis.
63 ukin (Il)-18 and gasdermin D (Gsdmd)-induced pyroptosis.
64 y cytokines IL-1beta and IL-18 and promoting pyroptosis.
65 sdermin D (GSDMD), an essential component of pyroptosis.
66 endocytosis, phagocytosis, inflammation, and pyroptosis.
67 ion receptor driving HBoV1 infection-induced pyroptosis.
68 interleukin-1beta (IL-1beta) and macrophage pyroptosis.
69 avage of pro-IL-1beta to active IL-1beta and pyroptosis.
70 uboptimal inflammatory milieu in the case of pyroptosis.
71 mediated inflammatory cytokine secretion and pyroptosis.
72 mbrane, resulting in lytic cell death called pyroptosis.
73 IL-18 and an inflammatory cell death called pyroptosis.
74 and induction of proinflammatory cell death pyroptosis.
75 interleukin-1 release, but only LPS induces pyroptosis.
76 a and IL-18, and a form of cell death termed pyroptosis.
77 of an inflammatory form of cell death called pyroptosis.
78 erminal fragment disrupted for inducing cell pyroptosis.
79 virus infection-apoptosis, necroptosis, and pyroptosis.
80 ll as a special type of cell death, known as pyroptosis.
81 allmark of a novel form of cell death termed pyroptosis.
82 o secretion of proinflammatory cytokines and pyroptosis.
83 uced inflammatory cell death, referred to as pyroptosis.
84 ry responses and a form of cell death termed pyroptosis.
85 zation, membrane binding, pore formation and pyroptosis.
86 ts in proinflammatory cytokine signaling and pyroptosis.
87 ugh caspase-1-mediated cell death, known as "pyroptosis."
88 with flow cytometry to detect apoptosis and pyroptosis; 26% were pyroptotic (Caspase-1-positive).
89 ukin 1beta (IL-1beta) and IL-18, as well as 'pyroptosis', a form of cell death induced by bacterial p
90 tory bias of human keratinocytes to activate pyroptosis, a caspase 1-dependent form of inflammatory c
91 chemical and cellular mechanisms controlling pyroptosis, a Caspase-1/11 dependent form of cell death
92 elds an N-terminal p30 fragment that induces pyroptosis, a death program important for the eliminatio
93 nes interleukin-1beta and interleukin-18 and pyroptosis, a form of phagocyte cell death induced by ba
97 Sensing of these DNA fragments results in pyroptosis, a highly inflammatory form of programmed cel
99 lso protects against infection by triggering pyroptosis, a proinflammatory and lytic mode of cell dea
103 ns unclear whether PARP1 is processed during pyroptosis, a specialized cell-death program that occurs
104 ptosome formation, which in turn leads to AM pyroptosis, a type of caspase-1-dependent inflammatory c
105 dergo a very rapid form of cell death termed pyroptosis after activating the protease caspase-1.
107 hages) to carbon black nanoparticles induces pyroptosis, an inflammasome-dependent form of cell death
109 ffector-triggered PCD is partly analogous to pyroptosis, an inflammatory host cell death process that
111 1beta-IL-1RI signaling is responsible for AM pyroptosis and augmented lung injury in response to LPS.
112 by inhibiting caspase-1-dependent macrophage pyroptosis and augments host tolerance by controlling in
114 ice implicated a role for caspase-1-mediated pyroptosis and confirmed that CAPS is inflammasome depen
115 n an inflammasome complex, caspase-1 induces pyroptosis and converts pro-IL-1beta and pro-IL-18 into
116 om affected individuals are polarized toward pyroptosis and exhibit abnormal staining for inflammasom
117 nt proteins within GSDMD that support native pyroptosis and facilitate live-cell imaging of pyroptoti
118 this inflammasome induces pore formation and pyroptosis and facilitates the restriction of bacterial
119 he genetic architecture of susceptibility to pyroptosis and identifying unknown regulatory mechanisms
120 tributes to NAIP5/NLRC4 inflammasome-induced pyroptosis and IL-1alpha and IL-1beta production in resp
121 yperinflammation associated with M1-mediated pyroptosis and IL-1beta release could aggravate tissue i
122 trate required for efficient NLRP3-triggered pyroptosis and IL-1beta release, was not essential for M
123 nducing a pro-inflammatory cell death termed pyroptosis and in promoting the secretion of pro-inflamm
124 n chromosome 18 is associated with decreased pyroptosis and increased expression of TUBB6 (tubulin, b
125 clearance mechanism in the spleen, but both pyroptosis and interleukin-18 (IL-18)-driven natural kil
127 inflammasome-mediated caspase-1 activation, pyroptosis and interleukin-1beta secretion by soluble an
128 ted by gene targeting also exhibit defective pyroptosis and interleukin-1beta secretion induced by cy
129 and was associated with increased apoptosis/pyroptosis and mortality in a murine model of acute pneu
130 ial emphasis on lytic cell death pathways of pyroptosis and necroptosis and their implications in inf
132 d potassium efflux contribute to HIV-induced pyroptosis and NLRP3 inflammasome activation in podocyte
133 ulting amino-terminal fragment promotes both pyroptosis and NLRP3-dependent activation of caspase-1 i
134 monella enterica serovar Typhimurium-induced pyroptosis and proinflammatory cytokine secretion in mac
135 ant functions beyond the direct induction of pyroptosis and proinflammatory cytokine secretion in the
136 in an ASC-dependent manner, leading to both pyroptosis and release of the proinflammatory cytokines
137 -/-) macrophages undergo normal LeTx-induced pyroptosis and secrete significant amounts of interleuki
138 nical inflammasome activation and suppressed pyroptosis and secretion of IL-1alpha and IL-1beta induc
139 s completely blocked the effect of AgNP15 on pyroptosis and secretion of IL-1beta, indicating that AT
140 ch recognizes intracellular LPS and promotes pyroptosis and secretion of proinflammatory cytokines.
141 ath effector mechanism of caspase-1-mediated pyroptosis and support the notion that this pathway of p
142 exin-1 and P2X7 downstream of caspase-11 for pyroptosis and susceptibility to sepsis induced by the n
143 lecular and morphological characteristics of pyroptosis and the individual inflammasomes and their co
145 (GSDMD-NT) that triggers inflammatory death (pyroptosis) and release of inflammatory cytokines such a
147 vation is important for release of alarmins, pyroptosis, and early IFN-gamma production by memory CD8
148 n the mechanisms underlying caspase-mediated pyroptosis, and have implications for the development of
150 cluding immunogenic cell death, necroptosis, pyroptosis, and netosis that interweave different cell d
152 caspase-11 was required for pore formation, pyroptosis, and restriction of Legionella replication in
153 tivate caspase-1-mediated cell death, called pyroptosis, and secretion of proinflammatory cytokines t
154 ity of RAW 264.7 cells to Salmonella-induced pyroptosis, and the endogenous expression of GBP-5 is im
157 aberration, drives activation of caspase-1, pyroptosis, and the release of the pro-inflammatory cyto
158 ecretion of bioactive IL-1beta and IL-18 and pyroptosis, and thus launches a systemic immune and infl
159 cytosol, and to decrease Salmonella-induced pyroptosis/apoptosis that allows the DNA vaccine time to
160 induced secondary necrosis and GSDMD-induced pyroptosis are dependent on caspase activation, we propo
162 a MyD88, and we identify commensally induced pyroptosis as a potential innate immune effector in seve
163 dently of IL-1beta and IL-18 and establishes pyroptosis as an efficient mechanism of bacterial cleara
164 ity, increased mitochondrial damage augments pyroptosis, as indicated by enhanced plasma membrane per
165 fected cells underwent apoptosis rather than pyroptosis, as indicated by increased cleaved caspase-3
166 r1Delta and stp2Delta strains did not induce pyroptosis, as measured by caspase-1-dependent interleuk
168 , which has been shown to prevent macrophage pyroptosis, attenuated both cell killing by p30 in a 293
169 nse caused by IL-1beta and IL-18 rather than pyroptosis, because we observed augmented bacterial burd
171 RP3-dependent rapid caspase-1 activation and pyroptosis, both of which are compromised in IRAK-1-defi
172 t only expand the molecular understanding of pyroptosis but also enable its direct visualization.
174 cella-infected macrophages exhibited minimal pyroptosis but secreted IL-1beta, which was suppressed b
175 ation, interleukin (IL)-1beta secretion, and pyroptosis, but not Nlrc4 phosphorylation by cytosolic f
176 n shown to trigger caspase-11 activation and pyroptosis, but the cytoplasmic sensor for LPS and compo
177 Legionella activation of caspase-11 induced pyroptosis by a mechanism independent of the NAIP/NLRC4
178 d that the induction of caspase-11-dependent pyroptosis by cytoplasmic L. pneumophila-derived LPS req
181 lack nanoparticle exposure was identified as pyroptosis by the protective effect of a caspase 1 inhib
182 racting protein 1 [RIP1] and RIP3 mRNAs) and pyroptosis (caspase 1, interleukin 1beta [IL-1beta], and
183 ivated caspase-1 protein, demonstrating that pyroptosis contributes to CD4(+) T cell death in vivo in
188 nce of ASC resulted in IL-1beta cleavage and pyroptosis, despite the absence of caspase-1 autoprocess
190 en by CD4 T cell depletion, mostly involving pyroptosis elicited by abortive HIV infection of CD4 T c
192 n overview of recent developments within the pyroptosis field, beginning with the discovery of Gasder
196 and inflammatory environments attenuates EC pyroptosis, improves EC survival mediated by vascular en
201 release of interleukin-1beta (IL-1beta), and pyroptosis in LPS-activated macrophages infected with wi
202 previous reports showing that NLRP1 enhances pyroptosis in macrophages, NLRP1 in melanoma behaved dif
204 he central role of inflammatory caspases and pyroptosis in mediating immunity to infection and cleara
207 nown for inducing inflammasome formation and pyroptosis in myeloid cells, increasing evidence highlig
209 lammatory signaling, IL-1beta production and pyroptosis in primed murine bone marrow-derived macropha
210 dy now highlights the specific importance of pyroptosis in resistance to intracellular pathogens.
211 tory cytokines and danger signals as well as pyroptosis in response to infections and cellular stress
212 d-type NLRC4, did not activate caspase-1 and pyroptosis in response to S. typhimurium, indicating tha
214 ally, our study demonstrates CIRP-induced EC pyroptosis in the lungs of C57BL/6 mice for the first ti
216 rting; FACS) strategy to detect and quantify pyroptosis in vivo based on detection of active caspase
218 maturation of IL-1beta and IL-18, as well as pyroptosis, in response to synthetic double-stranded DNA
219 o induce a new type of programed cell death, pyroptosis, in T lymphocytes through induction of Nod-li
220 essing; however, neutrophils did not undergo pyroptosis, indicating that K(+) efflux and IL-1beta pro
232 from host immune cells; instead, macrophage pyroptosis is driven by fungal cell-wall remodelling and
236 ood-derived CD4 T cells become sensitized to pyroptosis, likely recapitulating interactions occurring
237 inflammasome activation is closely linked to pyroptosis, lytic cell death did not occur following C.
239 showed that chronic inflammation induced by pyroptosis may facilitate persistence of the HIV latent
240 We propose that IL-1beta release without pyroptosis may occur in early-recruited monocytes to reg
241 in early SIV infection, which suggests that pyroptosis may play a pivotal role in the pathogenesis o
242 uggest that NMII-induced caspase-1-dependent pyroptosis may require its T4SS and activation of the TL
243 the use of caspase-1 inhibitors that inhibit pyroptosis, may maintain the CD4+ T cell population and
244 h of wild type (WT) BMDC via NLRP3-dependent pyroptosis, nigericin-stimulated Casp1/11(-/-) BMDC exhi
245 SIV, and by extension, that of HIV-1, since pyroptosis not only induces CD4(+) T cell death but also
246 prevented both ATP- and nigericin-triggered pyroptosis of human THP-1 cells in a time- and concentra
248 macrophages, and E. tarda infection triggers pyroptosis of infected macrophages from mice and fish an
249 of infection, whereas inflammasome-mediated pyroptosis of macrophages releases bacteria for uptake b
251 ving these cells with a LF and/or inhibiting pyroptosis of the cells can be a new therapeutic approac
255 of latently infected cells brought about by pyroptosis, or to a lesser extent by superinfection, mig
256 We conclude that apoptosis, necroptosis, and pyroptosis participate simultaneously during MAIDS-relat
257 otic or necrotic pathway; involvement of the pyroptosis pathway has not been reported previously.
258 terleukin 1beta [IL-1beta]) in the canonical pyroptosis pathway were significantly upregulated in exp
259 Importantly, genes involved in the canonical pyroptosis pathway were significantly upregulated, and t
266 acologic inhibition of NLRP3 or NOX suppress pyroptosis, ROS generation, and nuclear beta-catenin in
268 L-1beta but also provided protection against pyroptosis, suggesting that HIV-induced podocyte injury
269 aspase-1 maturation, IL-1beta secretion, and pyroptosis, suggesting that it retained Nlrc4 Ser533 pho
270 els of latency that do not take into account pyroptosis, superinfection, or other potential complexit
271 D (Gsdmd)-dependent lytic cell death called pyroptosis that promotes antimicrobial host defense but
272 C. muridarum infections induce GBP-dependent pyroptosis through both caspase-11-dependent noncanonica
273 s, such as Salmonella, must prevent or delay pyroptosis to avoid being trapped in the PIT and subsequ
275 that most T cells in the tissue die through pyroptosis triggered by abortive infection, i.e., infect
279 ant, reduction in Nlrp3 inflammasome-induced pyroptosis was observed in PARP1 knockout macrophages.
281 roinflammatory programmed cell death termed "pyroptosis." We demonstrate active caspase-1 diffusely d
282 d caspase-1 protein, the hallmark of ongoing pyroptosis, were significantly increased, which is corre
283 ein (MLKL) in necroptosis and gasdermin-D in pyroptosis] were recently discovered, bringing us closer
284 lammatory macrophage) and caused cell death (pyroptosis), whereas M-Mvarphi (resting macrophage) did
286 ccharide (LPS) leads to caspase-11-dependent pyroptosis, which is critical for induction of endotoxic
287 bial infection of immune cells often induces pyroptosis, which is mediated by a cytosolic protein com
288 nitiates the inflammatory cell death program pyroptosis, which is protective against numerous pathoge
289 NLRP1 inflammasome is sufficient to initiate pyroptosis, which subsequently leads to a self-amplifyin
290 ologically with paclitaxel (Taxol) increases pyroptosis without affecting the other major readout of
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