ライフサイエンスコーパス: LPS

1 LPS administration induced an inflammatory response in t

2 LPS induced similar activation of NF-kappaB, and stimula

3 LPS may be responsible for platelet activation and poten

4 LPS significantly correlated with zonulin (r = 0.45, P <

5 LPS-activated microglia exhibited a sialidase activity t

6 LPS-induced NF-kappaB reporter activity and intracellula

7 LPS-induced phagocytosis of primary neurons by primary m

8 LPS-induced release of the proinflammatory marker tumor

9 LPS-mediated activation of Toll-like receptor 4 (TLR4) i

10 LPS-responsive beige-like anchor protein (LRBA) and cyto

11 In a LPS-induced model of infection-associated PTB, 101.10 pr

12 d Aa serotype b lipopolysaccharide (LPS) (Aa-LPS), heat-killed (HK) bacteria (Aa-HK), or live bacteri

13 tinates NALP7 and STAMBP knockdown abrogates LPS or Pam3CSK4-induced increases in NALP7 protein.

14 Loss of rfaH affected LPS synthesis in both species, resulting in a shorter co

15 nd TLR-4 while increased that of IL-10 after LPS stimulation.

16 symptoms were assessed hourly till 8 h after LPS injection.

17 Three hours after LPS administration, blood was collected, and serum was t

18 re, genotype differences were observed after LPS exposure.

19 andidate target for developing drugs against LPS-induced septicemia.

20 orchestrate an inflammatory response against LPS and expressed three factors reported to control the

21 phage cells challenged with the TLR4 agonist LPS and TLR2 agonists lipoteichoic acid and zymosan.

22 m3CSK4 or FSL-1, as well as the TLR4 agonist LPS in the absence of additional ATP.

23 1beta release stimulated by the TLR4 agonist LPS is independent of both pannexin-1 and P2X7 activatio

24 KLF2 overexpression ameliorates LPS-induced lung injury in mice.

25 Because of the presence of amphipathic LPS molecules, the OM behaves as an effective permeabili

26 kidneys and cultured podocytes following an LPS challenge.

27 permeability, the mechanisms that mediate an LPS-induced increase in intestinal TJ permeability remai

28 c targeting of these pathways can prevent an LPS-induced increase in intestinal permeability.

29 EBP acted synergistically with TNF-alpha and LPS to induce CXCL1-proximal promoter activity.

30 lia are sexually dimorphic in both basal and LPS-induced activation and contribute to the sexually di

31 d functional analysis of CD14(+) CD1c(+) and LPS-activated CD14(+) CD1c(+) TSLPR(+) mono.

32 flagellar assembly, bacterial chemotaxis and LPS synthesis were enriched in the tumors while those re

33 the outer membrane-derived lipoproteins and LPS to inhibit TLR2 and TLR4 activation, respectively.

34 ial response of human leukocytes to MPLA and LPS has not been well characterized.

35 tibility to cecal ligation and puncture- and LPS-induced sepsis, which correlated with significantly

36 mined the spatiotemporal dynamics of RNA and LPS in retinal axons during arborization in vivo.

37 mic, associated with an increase in arterial LPS and a susceptibility to sepsis.

38 pon exposure to inflammatory factors such as LPS, thrombin, and TNFalpha, as has been observed in viv

39 DMP attenuated LPS-induced MAPK activation in BV2 cells, suggesting the

40 DKO mice had a blunted response to bacterial LPS, resembling endotoxin tolerance.

41 inflammatory genes in response to bacterial LPSs stimulation.

42 ously been related to their capacity to bind LPS, we suggest a direct antagonist effect of calixarene

43 sma-derived factor H and efficiently blocked LPS-induced alternative pathway activation and hemolysis

44 ed microglial pro-inflammatory activation by LPS, through the inhibition of Iba1 expression, TNF-alph

45 wondered whether they might too be caused by LPS (and reversed by LBP).

46 ase of a signal transducer and model drug by LPS from F. tularensis vs Pseudomonas aeruginosa and by

47 led that the IL-1Ra upregulation elicited by LPS alone is PKA-independent, whereas the rolipram-enhan

48 ism of TLR3 up-regulation that is induced by LPS-TLR4 signaling in a dose- and time-dependent manner

49 and the levels of IL-6 secretion induced by LPS.

50 leads to an increased induction of NLRP3 by LPS, which is also accompanied by increased Caspase-1 an

51 ates the inflammatory response stimulated by LPS and attenuates the inflammatory impact of a high fat

52 g blood clotting can be affected strongly by LPS.

53 can be distinguished from those triggered by LPS, as both agents oppositely regulate the expression o

54 peritoneal macrophages stimulated ex vivo by LPS.

55 criptional program distinct from a classical LPS response, pointing to unique P. falciparum-induced a

56 ginosa and, for comparison, Escherichia coli LPS environments on the physical properties of the OMs a

57 egative is a unique lipid bilayer containing LPS in its outer leaflet.

58 a majority of sensory neurons and decreased LPS-dependent neuronal excitability in small diameter ne

59 Mutants defective in AlmEF-dependent LPS modification exhibit reduced fitness in vivo Here, w

60 of OprH show distinct behaviors in different LPS environments.

61 Injection of these mice with low-dose LPS resulted in elevated serum TNF levels compared with

62 tifies cholangiocyte EV communication during LPS stimulation, and demonstrates that the SCT/SR axis m

63 istent with the clinical observations (i.e., LPS upregulated Wnt5a and downregulated sFRP5).

64 r, after glomerular injury induced by either LPS or nephrotoxic serum, the podocyte GR knockout mice

65 Elevated LPS-stimulated-Treg percentage at age 6 was associated w

66 ts mouse PTBs induced by bacterial endotoxin LPS or progesterone receptor antagonist mifepristone mor

67 P170-specific small interfering RNA enhanced LPS-induced IL-6 and TNF-alpha expression.

68 siRNA-mediated knockdown of TRIM59 enhanced LPS-induced macrophage activation.

69 (Nb)-infected hRETNTg(+) mice after a fatal LPS dose compared with naive mice or Nb-infected hRETNTg

70 Fecal LPS was higher in IBS patients than in healthy subjects

71 of feeding, as reflected by increased fecal LPS and bacterial metabolites and concomitant higher pla

72 had improved IBS symptoms and reduced fecal LPS levels.

73 Finally, LPS caused similar inflammation and injury in previously

74 e conformational transitions of MsbA to flip LPS, and paves the way for structural characterization o

75 at the Rgs10 promoter is enhanced following LPS stimulation.

76 allowing low levels of expression; following LPS stimulation, the IRAK-M promoter is derepressed, and

77 are deacetylated in BV-2 microglia following LPS activation, and HDAC1 association at the Rgs10 promo

78 n (H3K4Me3) at the CDKN2A promoter following LPS-induced senescence.

79 Our study uncovers the structural basis for LPS recognition, delineates the conformational transitio

80 ncrease of ceramide (Cer) was a hallmark for LPS activation.

81 an alternating lateral access mechanism for LPS extraction.

82 nstrating that HDAC enzymes are required for LPS silencing of Rgs10 Furthermore, we used chromatin im

83 The results demonstrate a requirement for LPS in building arbor complexity and suggest a key role

84 We demonstrate that differently from LPS-mediated dimerization of the TLR4-MD2 complex, palmi

85 Collectively, FK866 could ameliorate GaIN/LPS and ConA-induced ALF through induction of autophagy

86 24, 12, and 0.5 h before treatment with GaIN/LPS and ConA.

87 LX103 treatment for up to 3 hours after GalN/LPS administration was still remarkably effective in blo

88 In GalN/LPS-treated mice, VLX103 decreased activation of both th

89 l mice given injections of SR9009 were given LPS and D-galactosamine to induce fulminant hepatitis an

90 cytokine profile associated with heightened LPS levels.

91 eature of T2D, and may be driven by 'hidden' LPS.

92 However, LPS more potently induces pro-inflammatory cytokine and

93 In LPS/ATP-stimulated bone marrow-derived macrophages (BMDM

94 gulating the expression level of IL-1beta in LPS induced macrophage cells, and to cause significant r

95 dently suppressed the release of IL-27p28 in LPS/TLR4-activated macrophages, which was independent of

96 nt, significant hearing loss was detected in LPS-exposed animals.

97 inuria at 8 months of age or a difference in LPS-induced albuminuria.

98 himpanzees exhibited marginal differences in LPS responses, human monocyte-derived macrophages killed

99 Our data show that TLR4 ligation in LPS-primed DCs, induced higher levels of both IDO isofor

100 To study the role of neutrophils in LPS-induced endotoxemia, we developed a new mouse model,

101 vation of non-canonical NF-kappaB pathway in LPS-conditioned DCs.

102 r to further investigate the role of RfaH in LPS synthesis, resistance to host defense peptides, and

103 mechanism for IL-10-mediated suppression in LPS-stimulated macrophages and that inhibited genes can

104 upstream regulators and pathways, including LPS, members of the TLR and PPAR families, NF-kappaB, an

105 n and acute neutrophilic response to inhaled LPS challenge in volunteers with asthma.

106 TAT-4BB inhibited LPS-induced calcium changes in a majority of sensory neu

107 added Wnt5a enhanced whereas sFRP5 inhibited LPS-induced inflammation, as monitored by interleukin 8

108 tivity of guanidinocalixarenes in inhibiting LPS toxic action has previously been related to their ca

109 imultaneously, the Lyn mutations blocked its LPS-induced accumulation in the raft fraction of RAW264

110 ation of peroxisomes blocked the TLR4 ligand LPS-induced proinflammatory response, as detected by the

111 Lipopolysaccharide (LPS) decreased food/water intake and body weight in etha

112 Lipopolysaccharide (LPS) is the component of Gram-negative bacteria that act

113 Lipopolysaccharide (LPS) surface charge and aggregation were unaltered in th

114 thanol diet and/or acute lipopolysaccharide (LPS).

115 d cytokine release after lipopolysaccharide (LPS) stimulation, and CTSD KO also reduced caspase-3 act

116 gastric discomfort, and lipopolysaccharide (LPS), a bacterial cell wall component that induces infla

117 h purified Aa serotype b lipopolysaccharide (LPS) (Aa-LPS), heat-killed (HK) bacteria (Aa-HK), or liv

118 ) agonism with bacterial lipopolysaccharide (LPS) and the synthetic acylated lipopeptide Pam3CSK4.

119 flect changes induced by lipopolysaccharide (LPS) activation.

120 ation that is induced by lipopolysaccharide (LPS).

121 or after stimulation by lipopolysaccharide (LPS).

122 ctional Escherichia coli lipopolysaccharide (LPS) O antigen regulator WbdD.

123 uced by Escherichia coli lipopolysaccharide (LPS), a Toll-like receptor (TLR)-4 agonist.

124 n detection of cytosolic lipopolysaccharide (LPS).

125 esponsible for detecting lipopolysaccharide (LPS) of Gram-negative bacteria, was immobilized on both

126 A-binding assay, and ii) lipopolysaccharide (LPS)-induced human monocyte release of tumor necrosis fa

127 (NF-kappaB and MAPKs) in lipopolysaccharide (LPS)-stimulated macrophages.

128 t chrysophanol inhibited lipopolysaccharide (LPS)-induced iNOS and COX-2 expression in the BV2 mouse

129 an endotoxin injection [lipopolysaccharide (LPS)].

130 demonstrate that in mice lipopolysaccharide (LPS)-induced lethality is prevented by genetic ablation

131 y assessed the effect of lipopolysaccharide (LPS) administration at a dose of 2 ng/kg of body weight

132 ed by elevated levels of lipopolysaccharide (LPS) and related markers, is a common occurrence in HIV

133 anasal administration of lipopolysaccharide (LPS) or saline three times per week, and were immunohist

134 volved administration of lipopolysaccharide (LPS) to HIV transgenic (Tg) rats followed by assessment

135 A blocks the ability of lipopolysaccharide (LPS) to suppress Rgs10 transcription in BV-2 and primary

136 g the resolving phase of lipopolysaccharide (LPS)-induced inflammation when resolving macrophages pre

137 ion in a murine model of lipopolysaccharide (LPS)-induced periodontal disease.

138 pheral administration of lipopolysaccharide (LPS).

139 ntravenous injections of lipopolysaccharide (LPS, 3 mg/kg per week) to induce pancreatitis or saline

140 IFN-gamma or lipopolysaccharide (LPS) polarizes macrophages toward the M1, or "classicall

141 ipoprotein 1 [FSL-1]) or lipopolysaccharide (LPS) significantly induced proinflammatory mediators in

142 In particular, lipopolysaccharide (LPS) induces expression of MsrB1, but not other Msrs.

143 matory effects, reducing lipopolysaccharide (LPS)-stimulated ROS, nitric oxide and TNFalpha productio

144 Systemic lipopolysaccharide (LPS) is implicated in increasing mortality in patients w

145 Lipid A anchors the lipopolysaccharide (LPS) to the outer membrane and is usually composed of a

146 inhibits the response to lipopolysaccharide (LPS) by a pathway that apparently requires low-density l

147 s on immunoreactivity to lipopolysaccharide (LPS) stimulation, and cognitive function were assessed.

148 s of IL-8 and CCL-2 upon lipopolysaccharide (LPS)-stimulation.

149 lammatory bacterial wall lipopolysaccharide (LPS).

150 ble renitence," in which lipopolysaccharide (LPS) activation of macrophages protected their endolysos

151 a septic challenge with lipopolysaccharide (LPS) by 2-fold.

152 cted to stimulation with lipopolysaccharide (LPS) in the presence or absence of MSU.

153 ages were incubated with lipopolysaccharide (LPS) to induce expression of NLRP3, IL1B, and IL18; cell

154 giocytes stimulated with lipopolysaccharide (LPS), which is a membrane component of gram-negative bac

155 roinflammatory stimulus (lipopolysaccharide [LPS] from Porphyromonas gingivalis) in a manner consiste

156 d in mouse models of both lipopolysaccharide(LPS)-induced shock (LPSS) and hemorrhagic shock (HS).

157 te (PPH) by attenuating lipopolysaccharide- (LPS) induced pro-inflammatory gene expression in THP-1 m

158 S exposure, plus airway Lipopolysaccharides (LPS) inhalation, in building our COPD mouse model.

159 importance of Bp and Bm lipopolysaccharides (LPS) as vaccine candidates.

160 r's periplasmic domains.Lipopolysaccharides (LPS) are synthesized at the periplasmic side of the inne

161 tive bacteria, elevates lipopolysaccharides (LPS), and induces intestinal pathology, as indicated by

162 stigated the effects of lipopolysaccharides (LPS) and interleukin (IL)-17A on the activation of macro

163 cattering, we show that lipopolysaccharides (LPS) form bilayers that interact with PhiX174 at an icos

164 putative effectors, and lipopolysaccharides (LPSs), as well as other important traits likely to contr

165 azine in patients with advanced liposarcoma (LPS) or leiomyosarcoma showed a significant improvement

166 1013, and 22 genes were upregulated for LTA, LPS, Poly(dT), and Poly(I:C), and 12, 142, 249, and 16 g

167 49, and 16 genes were downregulated for LTA, LPS, Poly(dT), and Poly(I:C), respectively, with at leas

168 tors, and EPAC are prerequisites for maximal LPS-induced IL-33 expression and that exogenous PGE2 can

169 We found that Nox4 mediated LPS-TLR4 signaling in hepatocytes via NF-kB and AP-1 pat

170 erefore, our data suggest that Nox4 mediates LPS-TLR4 signaling in human hepatoma cells and murine he

171 with TsSPs and commercial PGE2 in modulating LPS-induced expression of many cytokines and chemokines

172 cription, as well as boosting the ability of LPS to induce IL-1beta mRNA and pro-IL-1beta while inhib

173 tocytes and may contribute to the ability of LPS to stimulate liver pathology.

174 In contrast, addition of LPS directly to latently infected monocytes was not suff

175 t physiologically relevant concentrations of LPS (0 to 1 ng/mL) cause an increase in intestinal epith

176 if IL-10 is included early in the course of LPS stimulation and is strongly enriched for IFN-inducib

177 of insulin with otherwise sublethal doses of LPS induced hypoglycemic shock in mice within 1-2 h.

178 tosis and override the prosurvival effect of LPS via annexin A1.

179 Effects of LPS on fibrogenic hepatic stellate cells (HSCs) from WT

180 The enhancement of LPS-induced liver damage by ethanol preexposure was asso

181 y (ELISA) performed on supernatant fluids of LPS challenged MDM showed ImI-mediated upregulation of p

182 thermore, miR-718 regulates the induction of LPS tolerance in macrophages.

183 ture as well as intraperitoneal injection of LPS.

184 ice were given intraperitoneal injections of LPS to induce peritoneal inflammation; plasma samples we

185 kely reflecting decreased systemic levels of LPS and C5a.

186 We found an increase in the levels of LPS and markers of monocyte activations in ED.

187 drinks in the past 30 days, higher levels of LPS, sCD14 and sCD163.

188 detailed role of CXCR7 in a murine model of LPS inhalation.

189 In the presence of LPS together with iC3b or fibrinogen, the expression lev

190 skin lesions and reveal the significance of LPS in OVA used in most studies, thus mimicking natural

191 the LptB2FG complex during the first step of LPS transport to the outer membrane.

192 ed no substantial change to the structure of LPS in the presence of OligoG CF-5/20, however, isotherm

193 , and this is associated with suppression of LPS-induced enhancer activation.

194 d comprehensive anti-inflammatory effects on LPS, ox-LDL or cholesterol crystal-induced NF-kappaB, c-

195 We show that TNF-alpha, but not IL-1beta or LPS, promoted nuclear enrichment of TonEBP protein.

196 transfer arthritis model and in IL-1beta- or LPS-induced systemic inflammation in vivo, IL-1R2(-/-) m

197 stimuli, such as high-NaCl concentration or LPS, exacerbated the mitochondrial damage and dysfunctio

198 Mesenteric lymphatic vessels from MetSyn or LPS-injected rats exhibited impaired intrinsic contracti

199 we challenged Lcn2(-/-) mice with peripheral LPS and determined effects on behavior and neuroinflamma

200 of E. coli RA101295 treatment reduced plasma LPS content in E. coli-challenged baboons, implying redu

201 ), or poly(I:C) significantly reduced plasma LPS-elicited proinflammatory cytokines, reflecting endot

202 Two hours post LPS, sickness-like behaviors increased, the transcriptio

203 red with placebo, gammaT notably reduced pre-LPS challenge sputum eosinophils and mucins, including m

204 Prolonged LPS-induced activation of p38 and JNK, phosphorylation o

205 ontaining exosomes is important for a proper LPS response.

206 In addition, miR-424 and miR-503 reduced LPS induced EC sprouting, migration and tube formation.

207 and mucins, including mucin 5AC and reduced LPS-induced airway neutrophil recruitment 6 and 24 hours

208 IL-8, TNF-alpha and COX-2, while PPH reduced LPS-induced IL-6 and TNF-alpha responses.

209 e-dependent; following six weeks of repeated LPS stimulation in vivo, hepatic TNF-alpha and PCNA resp

210 cally incorporates into rough and deep-rough LPS.

211 Serum LPS, sCD14, and sCD163 were measured.

212 The levels of serum LPS, sCD14, and sCD163 were higher among ED with recent

213 were taken from the same donors when "sick" (LPS-injected) and when "healthy" (saline-injected) and s

214 nally, plasma cell differentiation of sorted LPS-stimulated MZ B cells was impaired, and aged bumble

215 We found that proinflammatory stimulants LPS, IL-6 and IL-1beta up-regulated the expression of HC

216 provide evidence that inflammatory stimuli (LPS) can also control the expression of Trem1 independen

217 xpression of TRIM59 significantly suppressed LPS-induced macrophage activation, whereas siRNA-mediate

218 Nox4 silencing suppressed LPS-induced TNF-alpha and PCNA increases in human cells.

219 how that CsgB, in the presence of surfactant/LPS, accelerates the fibrillation rate of CsgA by circum

220 xity and suggest a key role for pre-synaptic LPS in assembling neural circuits.

221 We also demonstrate that LPS activates the transcription factor XBP1 via the ER s

222 We found that LPS-activated BV-2 microglia rapidly released Gal-3, whi

223 our in vitro senescence model, we found that LPS-induced CDKN2A expression coincided with a 4.5-fold

224 In line with this, we found that LPS-stimulated human monocytes released relatively low l

225 The results further indicate that LPS signaling in activated HSCs might be a mechanism of

226 We show that LPS exposure of C57BL/6 WT mice constraints IgE-MC-media

227 We suggest that LPS-induced changes in motivation may be due to alterati

228 Collectively, these studies suggest that LPS-induced IL-10 promotes the down-regulation of MC sur

229 The LPS-induced increase in intestinal permeability was inhi

230 The LPS-induced increase in mouse intestinal permeability al

231 kinase phosphorylation, which attenuated the LPS/GaIN-induced hepatic inflammation in the mice.

232 culture, we demonstrate that hRetn binds the LPS receptor Toll-like receptor 4 (TLR4) through its N t

233 ivefold channel at the vertex contacting the LPS.

234 es Apt/AuAC/Au an excellent platform for the LPS detection.

235 Results In the LPS subgroup, OS was significantly improved: 15.6 versus

236 RNA-induced knock-down of MLCK inhibited the LPS-induced increase in Caco-2 TJ permeability.

237 bunits and the transmembrane subunits of the LPS transporter.

238 The magnitude of the LPS-elicited cytokine response is commonly used to asses

239 In this study, we focus on the LPS-induced cytoplasmic circRNA, mcircRasGEF1B, and comb

240 howed that FPW extract is able to reduce the LPS-induced expression of pro-inflammatory genes IL-1bet

241 lammatory protein capable of suppressing the LPS-induced expression of inflammatory markers in vivo a

242 manner in AMPhi from C57BL/6 mice, while the LPS-induced TLR3 expression was significantly reduced in

243 en modal distribution and interacts with the LPS biogenesis machinery.

244 tion and bone resorption associated with the LPS model of experimental periodontal disease.

245 These LPS-derived EVs induce inflammatory responses in other c

246 Thus LPS stimulated monocytes are partially permissive lytic

247 production, when triggered by zymosan/TLR2, LPS/TLR4, or R848/TLR7/8 activation, but selectively spa

248 tion of other proinflammatory genes by TLR4 (LPS), TLR3 (polyriboinosinic-polyribocytidylic acid), TL

249 HDMECs) treated with TLR3 [Poly(I:C)], TLR4 (LPS), and TLR7 (imiquimod) agonists showed decreased pro

250 ll line RAW264.7 and human monocyte THP-1 to LPS from Porphyromonas gingivalis (PgLPS), an oral micro

251 NADPH oxidases contribute to LPS-induced reactive oxygen species (ROS) production and

252 derstanding how ATP hydrolysis is coupled to LPS transport.

253 tlr4(-/-) and IL10(-/-) mice were exposed to LPS, and serum cytokines (TNF and IL-10) were measured.

254 Yet, when exposed to LPS, GR knockout podocytes demonstrated fewer stress fib

255 pletion of RNF146 caused hypersensitivity to LPS-induced TNF-alpha production in vivo.

256 ten-day alcohol feeding primed the liver to LPS-induced lipid accumulation and liver injury with sig

257 acinar cells and sensitized the pancreas to LPS-induced pathology.

258 Procalcitonin reacted to LPS insult late.

259 okines and nitric oxide (NO), in response to LPS and alpha-synuclein.

260 (+) monocyte CCL17 production in response to LPS and IL-4.

261 ECP and histamine production in response to LPS by ELISA.

262 iR-503 have augmented angiogenic response to LPS in a Matrigel plug assay.

263 bese mothers generate a dampened response to LPS stimulation compared with those born to lean mothers

264 essed the induction of IRAK-M in response to LPS stimulation.

265 its function during the cellular response to LPS stimulation.

266 dogenous tPA increased 3-fold in response to LPS, to 116 +/- 15 pM, but remained below the approximat

267 defense and for the cold-seeking response to LPS, we studied rats with small thermal lesions in diffe

268 d to ameliorate the inflammatory response to LPS.

269 induce p-FOXO3 and apoptosis in response to LPS.

270 ed in a temperature elevation in response to LPS.

271 inflammatory cytokine release in response to LPS.

272 y reduced inflammatory cytokine responses to LPS and bacterial infection, POP2 transgenic mice are mo

273 y, and 8 weeks later, they were subjected to LPS (2 mg/kg) or sepsis by cecal ligation and puncture (

274 MSC-derived EVs before adoptive transfer to LPS-injured mice.

275 nclusion In patients with previously treated LPS, eribulin was associated with significantly superior

276 The truncated LPS were identified as Kdo-N3-lipid IVA and (Kdo-N3)2-li

277 vivo decreased from age 4.5 to 6 years (P(U,LPS) < 0.001; P(PI) = 0.051; P(FOXP3) < 0.001).

278 ns or of the cysteine residue that undergoes LPS-induced palmitoylation.

279 Unlike LPS, palmitate exposure does not activate STAT1, and its

280 Upon LPS challenge, serum levels of TNF-alpha, KC, IL-6, and

281 was also induced in the spleens of mice upon LPS injection.

282 fractionation experiments revealed that upon LPS stimulation of macrophages, CLIC1 and CLIC4 transloc

283 t expresses the highest levels of TSLPR upon LPS stimulation.

284 Experiments using LPS-activated primary macrophages revealed that the anti

285 ay be elicited in an analogous fashion using LPS in bone marrow-derived macrophages upon inhibition o

286 mice enhanced serum cytokine responses when LPS challenge occurred during the inactive phase (ZT0);

287 ted with LPS, Lcn2(-/-) mice challenged with LPS had exacerbated levels of pro-inflammatory cytokines

288 es in response to sequential challenges with LPS and Poly I:C, a TLR3 ligand, which was physiological

289 tration of dimethyl PGE2 in conjunction with LPS.

290 ce secreted more inflammatory cytokines with LPS stimulation and showed more phagocytic activity.

291 3, IL1B, and IL18; cells were incubated with LPS and adenosine triphosphate to activate the NLRP3 com

292 ected with LPS, Lcn2(-/-) mice injected with LPS had unique transcriptional profiles and significantl

293 duction in wild-type (WT) mice injected with LPS, Lcn2(-/-) mice challenged with LPS had exacerbated

294 Compared with WT mice injected with LPS, Lcn2(-/-) mice injected with LPS had unique transcr

295 Activation of leukocytes with LPS followed by treatment with the calcium ionophore A23

296 Priming of mice with LPS, monophosphoryl lipid A (MPLA), or poly(I:C) signifi

297 Priming microglia with LPS induced greater microglia activation in the PAG of f

298 n compared with dacarbazine in patients with LPS, an independently randomized stratified subgroup of

299 cytic capacity of human MDMs stimulated with LPS or ARDS BALF.

300 od from human volunteers was stimulated with LPS, MPLA or vehicle.