ライフサイエンスコーパス: LPS

1 LPS (250 ug/kg) induced hypoglycemia, which was mimicked

2 LPS activated mRNA expression of different pro-inflammat

3 LPS additionally promotes the physical and functional un

4 LPS also increased NLRP3 response in human hepatocytes,

5 LPS also increased SETD1 nuclear localization in a p65-d

6 LPS and DSP-4 decreased rotarod and wirehang activity, r

7 LPS can cause death as a result of septic shock, and its

8 LPS did not increase peroxisome proliferation-activated

9 LPS down-regulated expression of alphaSMA, PDGFbetaR, tr

10 LPS down-regulated the expression of cMyb, a transcripti

11 LPS drives neutrophil exhaustion through TICAM2 mediated

12 LPS further increased expression of TSPO and IL-6 in SNC

13 LPS induced phenotypic changes in aHSCs (rounding, size

14 LPS molecules are synthesized in the inner membrane and

15 LPS transcriptionally activates YAP through activator pr

16 LPS treatment in monogenic mutant mice did not induce am

17 LPS-induced expression of Il-10, Il-12 and Tnf-alpha was

18 LPS-induced miR-675-3p and -5p expression was Zip14-depe

19 LPS-induced pro-inflammatory stimulation suppressed Trem

20 LPS-induced release of IL-1beta but not TNF-alpha was fu

21 LPS-induced YAP further enhances expression of proinflam

22 LPS-stimulated primary human monocytes revealed specific

23 y, microtubule-destabilizing drugs abrogated LPS-induced IL18 expression, but this effect could be fu

24 asma membrane CD14 that functionally affects LPS, but not monophosphoryl lipid A, pro-inflammatory cy

25 o and upregulated NF-kappaB activation after LPS treatment, whereas treatment with a potent inhibitor

26 +/+) littermates at both baselines and after LPS challenge.

27 e recruitment of somatic cells in milk after LPS treatment was delayed by HS.

28 Mphis produced higher amounts of PGE2 after LPS stimulation compared with controls.

29 d N-acetylaspartate (NAA) were reduced after LPS, whereas glutamine was increased.

30 mma expression in the lung tissue alleviates LPS-/IgG immune complexes-stimulated acute pulmonary dam

31 t cannot produce KPS and displays an altered LPS structure.

32 us macaque model of IUI given intra-amniotic LPS, induction of p-IRAK1 and downstream proinflammatory

33 These findings characterize hGBP1 as an LPS-binding surfactant that destabilizes the rigidity of

34 physiological flow assays, we found that an LPS-primed endothelium synergistically enhanced neutroph

35 -beta, IFN-alpha2 and IL-7 in response to an LPS challenge.

36 ation in mice (female BALB/c strain) with an LPS-induced acute lung injury.

37 cal barrier, whereas lipid A moieties anchor LPS molecules.

38 and its expression was increased by IL-1 and LPS.

39 d fat mass and lean mass during cachexia and LPS-induced anorexia.

40 higher levels of IL-12p70 upon IFN-gamma and LPS stimulation than those from individuals without the

41 production and is involved in HH103 KPS and LPS biosynthesis and that an HH103 rkpM mutant cannot pr

42 In mice with NASH, LPS serum levels and LPS hepatocyte localization were increased compared with

43 ce of bacterial lipopolysaccharide (LPS) and LPS control factors such as soluble CD14 (sCD14) and end

44 tidylic acid-low-molecular-weight/LyoVec and LPS to evaluate IFN-alpha and TNF-alpha production capac

45 acetylated BSA [AcBSA], zymosan, mannan, and LPS from Escherichia coli and Salmonella as well as to t

46 weeks of exposure to either PM(2.5) (PM and LPS + PM group) or filtered air (control and LPS5w group

47 3 PUFA group a clear relation with serum and LPS-stimulated cytokines was not found but, unexpectedly

48 Since TolC and LPS contribute to antibiotic resistance, phage U136B sho

49 Both tolC and LPS-related mutants arise readily during fluctuation ass

50 DPLA elicited the same effects as LPS on aHSCs, indicating specificity, and monophosphoryl

51 eir tolerance for microbial stimuli, such as LPS and Poly I:C, resulting in increased production of k

52 r microvascular endothelial cells attenuated LPS-induced increases in ICAM1, VCAM1, IL8, and IL6 and

53 Importantly, the association between LPS levels, inflammation, and hematological dysfunction

54 to participate in outer-membrane biogenesis: LPS transport via the Lpt machine, and phospholipid tran

55 specific peptide efficiently mitigated both LPS/D-Galn- and ConA-induced liver injury and immune hyp

56 Here, we show that both LPS and interleukin (IL)-1beta trigger hypoglycemia, red

57 The plasma metabolites altered by LPS are involved in energy metabolism, including lipopro

58 flammatory ROS, cytokines, and chemokines by LPS-activated neutrophils.

59 the DUSP11-TAK1 interaction was enhanced by LPS stimulation in bone marrow-derived macrophages.

60 micutes/Bacteroidetes ratio was increased by LPS in SNCA mice.

61 t study, we determine whether ALI induced by LPS and IgG immune complexes is affected by C/EBPgamma.

62 In a model of acute lung injury induced by LPS, C6(-/-) mice showed reduced PMN buildup and less lu

63 genes previously unknown to be modulated by LPS to 24 h genes known to regulate angiogenesis/vasculo

64 ons (both sexes), its chronic stimulation by LPS induces a selective increase in the excitatory synap

65 tor expression, and independent of canonical LPS-induced intercellular feedback in the tumor necrosis

66 In long-term (23 h) tests chronic LPS also reduced licking responses to saccharin, sucrose

67 We conclude that circulating LPS can promote systemic inflammation and contribute to

68 -derived dendritic cells compared to E. coli LPS.

69 We studied Escherichia coli LPS in patients with biopsy-proven NAFLD, 25 simple stea

70 In NAFLD, Escherichia coli LPS may increase liver damage by inducing macrophage and

71 In conclusion, LPS induces a unique phenotype in aHSCs associated with

72 In contrast, LPS-induced systemic inflammation enhanced Zip14-depende

73 iscovered pro-inflammatory role of cytosolic LPS, our data reveal a distinct mode of LPS action that,

74 in protecting intestinal tissue from damage, LPS-induced weight loss, and leukocyte infiltration.

75 ant alkaline phosphatase (recAP) deactivates LPS.

76 Saa1 and Saa2 being comparable to high dose LPS.

77 ediated NLRP3 inflammasome activation during LPS transfection; however, its role in Gram-negative bac

78 y a transient cis-eQTL present only in early LPS response and lost before the trans effect appeared.

79 mulation with either TNF-alpha, IL-1beta, Ec-LPS, or Pg-LPS, increased the secretion of CSF-1 (P < 0.

80 sed the secretion of CSF-1 (P < 0.05) and Ec-LPS stimulation increased IL-34 (P < 0.05).

81 eta, Escherichia coli lipopolysaccharide (Ec-LPS) and Porphyromonas gingivalis lipopolysaccharide (Pg

82 eived an intraperitoneal injection of either LPS (0.83 mg/kg) or saline, and were assessed for depres

83 SLP-8348 was previously shown to enhance LPS-induced activation on both RAW264.7 macrophages and

84 At equivalent LPS doses, DDI consistently induced more PTB than SPI, a

85 sette (ABC) transporter LptB(2) FGC extracts LPS from the inner membrane and places it onto a peripla

86 Following LPS-mediated TLR2/4 activation, TNF-alpha and IL-1beta s

87 aggerated proinflammatory response following LPS/ATP stimulation.

88 ming protein Perforin-2 (P2) is critical for LPS-induced endotoxic shock in wild-type mice.

89 protein to the plasma membrane important for LPS signaling via TLR4.

90 ema3e(-/-) ) mice were better protected from LPS-induced acute inflammation as exemplified by their s

91 ore, IRAK1 knockout mice were protected from LPS-induced PTB, which was seen in wild-type controls.

92 Furthermore, LPS-induced plasma and brain [regions involved in autono

93 liver failure was induced with Galactosamine-LPS and in both models animals were treated with recAP p

94 atients had higher serum LPS and hepatocytes LPS localization than controls, which was correlated wit

95 Ab, NB6-228.22, that can recognize the HH103 LPS, but not those of most of the S. fredii strains test

96 However, LPS can also attenuate fibrogenic characteristics of aHS

97 CRISPR-Cas9 knockout screen that identified LPS-induced TNF-alpha factor (LITAF) as the HBL receptor

98 FOSL1 silencing impaired LPS-induced in vitro HPMEC angiogenesis.

99 nts for changes in cytokines in serum and in LPS-stimulated whole blood samples and leukocyte membran

100 Pdelta have been extensively investigated in LPS- and IgG immune complexes-stimulated acute lung inju

101 nd reduced oxidative stress (iNOS and NO) in LPS activated murine macrophages (RAW 264.7) by inhibiti

102 have shown caspase-8-mediated pyroptosis in LPS-activated macrophages but have provided conflicting

103 al, hydrogen peroxide levels were reduced in LPS-treated mCAT BMDMs.

104 In (LPS/ATP-stimulated) PBMCs, IL-18/TNF/caspase-1 were all

105 Ex vivo, MIA-690 and MR-409 inhibited LPS-induced inflammatory and pro-oxidative markers.

106 IAP also inhibited LPS-induced IL-1beta mRNA expression and activation of N

107 TMA and cadaverine inhibited LPS-stimulated TNF-alpha and IL-6 secretion by primary h

108 asome activation and, in doing so, inhibited LPS- and nigericin-induced assembly of the NLRP3 inflamm

109 ts, we confirmed vitamin D and VDR inhibited LPS- or activated CD4(+) T cell-induced miR-27a/b reduct

110 The data indicate that DUSP11 inhibits LPS-induced macrophage activation by targeting TAK1.

111 and platelet activation after intratracheal LPS or Pseudomonas aeruginosa challenge.

112 d lung injury in CF mice after intratracheal LPS or Pseudomonas aeruginosa challenge.

113 hybrid peptide were mainly attributed to its LPS-neutralizing activity and antagonizing the activatio

114 directly to LPS and induces "detergent-like" LPS clustering through protein polymerization.

115 Lipopolysaccharide (LPS) O-antigen (O-Ag) is known to limit antibody binding

116 Lipopolysaccharide (LPS) resides in the outer membrane of Gram-negative bact

117 Lipopolysaccharide (LPS), a component of the outer membrane of gram-negative

118 Lipopolysaccharide (LPS), a toxic byproduct of bacterial lysis, has been ext

119 Lipopolysaccharide (LPS), an inflammatory stimulus derived from gram-negativ

120 Lipopolysaccharide (LPS)-mediated intestinal damage, driven by STAT1-induced

121 , the inflammatory agent lipopolysaccharide (LPS), or both.

122 l elastase and aggregate lipopolysaccharide (LPS) and the Gram-negative bacterium Escherichia coli Ho

123 ictable stress (CUS) and lipopolysaccharide (LPS) models.

124 gue, the protein Ail and lipopolysaccharide (LPS)(6) enhance lethality by promoting resistance to hum

125 Escherichia coli O111:B4 lipopolysaccharide (LPS) associated with sepsis shock in microliter samples.

126 gram-negative bacteria, lipopolysaccharide (LPS), binds NLRP6 directly and induces global conformati

127 he presence of bacterial lipopolysaccharide (LPS) and LPS control factors such as soluble CD14 (sCD14

128 th gut-derived bacterial lipopolysaccharide (LPS) are implicated in hepatic fibrogenesis.

129 LR2/4 agonist, bacterial lipopolysaccharide (LPS).

130 asma levels of bacterial lipopolysaccharide (LPS).

131 ddition, increased blood lipopolysaccharide (LPS) levels during SIV infection were reduced to near no

132 ailure models induced by lipopolysaccharide (LPS) plus D-galactosamine (D-Galn), and concanavalin A (

133 mune response to E. coli lipopolysaccharide (LPS) could be conditioned by heat stress (HS).

134 activation by cytosolic lipopolysaccharide (LPS) causes pyroptotic cell death facilitated by gasderm

135 te secretion, detoxifies lipopolysaccharide (LPS), regulates gut microbes, and dephosphorylates proin

136 ized bacterial endotoxin lipopolysaccharide (LPS) activated the pore-forming protein Gasdermin D, whi

137 lated with the endotoxin lipopolysaccharide (LPS).

138 date a revised model for lipopolysaccharide (LPS)-induced macrophage activation that invokes a mechan

139 interferon (IFN)-gamma, lipopolysaccharide (LPS), and adenosine receptors.

140 Our data identified lipopolysaccharide (LPS) as a bona fide effector caspase inhibitor that dire

141 -1-dependent IL-1beta in lipopolysaccharide (LPS)-primed mouse bone marrow-derived dendritic cells (B

142 2+ influx, which induces lipopolysaccharide (LPS) internalisation, followed by activation of caspase-

143 is recruited to maturing lipopolysaccharide (LPS)-containing phagosomes in an adaptor protein-3 (AP-3

144 tion of glycine-modified lipopolysaccharide (LPS) and depletion of outer membrane porin OmpT, which c

145 ice with graded doses of lipopolysaccharide (LPS) and various inhibitors to evaluate the role of vari

146 n the lipid A portion of lipopolysaccharide (LPS) for the enteric pathogens Yersinia pseudotuberculos

147 a, O-antigen segments of lipopolysaccharide (LPS) form a chemomechanical barrier, whereas lipid A moi

148 ne circulating levels of lipopolysaccharide (LPS) in control and CRC populations.

149 sion under conditions of lipopolysaccharide (LPS) pro-inflammatory or IL-4 anti-inflammatory stimulat

150 under the stimulation of lipopolysaccharide (LPS), KCl and oxygen/glucose deprivation (OGD) that refl

151 vivo in a mouse model of lipopolysaccharide (LPS)-induced acute lung injury (ALI).

152 ponse to lethal doses of lipopolysaccharide (LPS).

153 by the administration of lipopolysaccharide (LPS).

154 th a single injection of lipopolysaccharide (LPS).

155 njection of high dose of lipopolysaccharide (LPS).

156 ts of SIRT7 depletion on lipopolysaccharide (LPS)-induced inflammatory responses and endothelial barr

157 th palmitate (PA) and/or lipopolysaccharide (LPS).

158 permeability, and plasma lipopolysaccharide (LPS) levels.

159 surface of OmpF and that lipopolysaccharide (LPS) enhances this binding.

160 Here, we showed that lipopolysaccharide (LPS) in combination with IFN-gamma inhibited PINK1-depen

161 re also confirmed in the lipopolysaccharide (LPS)- or activated CD4(+) T cell-treated human oral kera

162 In vivo, responses to lipopolysaccharide (LPS) result in IL-1beta secretion.

163 roteins in comparison to lipopolysaccharide (LPS), underlying the differences between pathogen-induce

164 ary cells in response to lipopolysaccharide (LPS).

165 y Salmonella typhimurium lipopolysaccharide (LPS).

166 Mice injected with lipopolysaccharide (LPS) display a depressive-like phenotype twenty-four hou

167 owed by stimulation with lipopolysaccharide (LPS).

168 anasally challenged with lipopolysaccharide (LPS).

169 x specimens treated with lipopolysaccharide (LPS).

170 y stimulating cells with lipopolysaccharide (LPS).

171 d an HFD or treated with lipopolysaccharide (LPS).

172 Lipopolysaccharides (LPS) are essential envelope components in many Gram-nega

173 septic molecules, e.g. lipopolysaccharides (LPS), cytokines and damage- or pathogen-associated molec

174 ipids and outer leaflet lipopolysaccharides (LPS).

175 itro with the prolonged lipopolysaccharides (LPS) stimulation can effectively develop an exhaustive p

176 -layer assembles on the lipopolysaccharides (LPS) of the cell surface.

177 peritoneal administration of liposaccharide (LPS), with Day 29 mice showing strong pathological respo

178 cytokine release into the airways upon local LPS instillation.

179 istone lysine methylation/demethylation of M(LPS + IFN-gamma)/M(IL-10) genes is one of the factors th

180 lly (i.n) instilled prior administering i.n. LPS.

181 In mice with NASH, LPS serum levels and LPS hepatocyte localization were in

182 nclude that GFAT2 should be considered a new LPS-inducible gene involved in regulation of protein O-G

183 rations, while exposure either to LPS or NNK/LPS in combination led to increased levels of global cyt

184 teria culture containing naturally occurring LPS, with similar recoveries in both cases.

185 eurons of the S1DZ eliminated the ability of LPS to reverse the sociability phenotypes in MIA offspri

186 activity and antagonizing the activation of LPS-induced Toll-like receptor 4-myeloid differentiation

187 The activity of LPS was reduced by recAP.

188 The i.p. administration of LPS to transgenic mice carrying a human SE-coding HLA-DR

189 tion on local and systemic administration of LPS.

190 pid A, the conserved and essential anchor of LPS.

191 mmetric character and unique biochemistry of LPS molecules contribute to the OM's ability to function

192 n skin, and IL-13 suppressed the capacity of LPS-stimulated human skin DCs to express IL-12 and promo

193 lipids, like cardiolipins, and components of LPS molecules, like lipid A endotoxins.

194 oligosaccharide (O)-antigenic determinant of LPS that S Typhi shares with S Enteritidis.

195 A single dose of LPS-induced a 10-fold increase in luciferase expression

196 sease following exposure to a lethal dose of LPS.

197 al analysis demonstrated that the effects of LPS on excitatory transmission are attributable to an in

198 uptake blunted the pro-injurious effects of LPS, suggesting a synergistic anti-inflammatory effect o

199 source of Saa3 in plasma after injection of LPS was adipose tissue rather than liver.

200 , we show that serial systemic injections of LPS (1 mg/kg, i.p., daily) for 4 consecutive days (LPSx4

201 ce of Escherichia coli by reducing levels of LPS and outer membrane integrity.

202 re, to further characterize the mechanism of LPS-induced secretion in vitro, we reveal an important r

203 ated rat HSCs were exposed to 0-100 ng/mL of LPS or its active component, diphosphoryl-lipid A (DPLA)

204 olic LPS, our data reveal a distinct mode of LPS action that, through the disruption of the early coo

205 Our study sheds light on the mystery of LPS-induced inflammasome initiation, reveals the archite

206 at Pf lessens the inflammatory phenotypes of LPS-activated neutrophils.

207 improved the reproducibility and potency of LPS in the model using two injections distal to the cerv

208 ence recovery is observed in the presence of LPS with a similar structure, illustrating the high sele

209 cally challenged with nanogram quantities of LPS to trigger lung vasoocclusion.Measurements and Main

210 tivation, imposing a consequent reduction of LPS-induced Il1b expression.

211 cted but essential role in the regulation of LPS biogenesis, presents a new structural basis for the

212 hosphomannose isomerase controls response of LPS-activated macrophages to D-mannose, which impairs gl

213 teoclast differentiation and activity and on LPS-induced expression of inflammation-associated genes.

214 ited microglial activation induced by CUS or LPS treatment.

215 n of glomerular disease (with Doxorubicin or LPS).

216 ct ligation and were injected with saline or LPS to mimic ACLF.

217 when MM6 cells were treated with zymosan or LPS during differentiation with TGF-beta and 1,25diOHvit

218 e were altered following a single peripheral LPS challenge that led to depressive-like behaviour in t

219 ynamics simulation and modeling, a pertussis-LPS-like pentasaccharide was chemically synthesized for

220 phyromonas gingivalis lipopolysaccharide (Pg-LPS) stimulation, using enzyme-linked immunosorbent assa

221 th either TNF-alpha, IL-1beta, Ec-LPS, or Pg-LPS, increased the secretion of CSF-1 (P < 0.05) and Ec-

222 ed mucosal permeability, and elevated plasma LPS; TJ disruption by TBI was more severe in Lpar2(-/-)

223 lammatory mediators following IFN-gamma plus LPS stimulation.

224 ured EGCs, co-incubation with palmitate plus LPS led to a significant increase in both SP and IL-1bet

225 essed the activation of microglia, prevented LPS-induced mitochondrial fragmentation in neurons, and

226 reduced aggregation following the prolonged LPS challenge as compared to wild type (WT) neutrophils.

227 rophil exhaustion triggered by the prolonged LPS challenge.

228 load, intestinal fatty acid-binding protein, LPS, and soluble LPS receptor soluble CD14 (sCD14).

229 P, protected against ALI induced by purified LPS.

230 f inflammatory markers in dams that received LPS DDI compared with LPS SPI.

231 to phosphorylate STAT3, and failed to reduce LPS induced inflammatory cytokines in the presence of ex

232 ontrolling bacterial infections and reducing LPS-induced inflammation are unclear.

233 nding of the bacterial factors that regulate LPS biogenesis is incomplete.

234 Remarkably, LPS-induced lethality was almost completely abrogated in

235 Antibiotic treatment of neonates restored LPS-induced small intestinal cell shedding, whereas adul

236 l uncouplers that promote mitophagy reversed LPS/IFN-gamma-mediated activation of macrophages and led

237 never been reported from any other rhizobial LPS.

238 NASH patients had higher serum LPS and hepatocytes LPS localization than controls, whic

239 TLR4(+) platelets correlated with serum LPS values.

240 atosis or controls and correlated with serum LPS.

241 , including NF-kB signaling, IL-6 signaling, LPS/IL-1-mediated inhibition of RXR Function, PI3K in B

242 tion of lipid A derived from intact (smooth) LPS from host-pathogen MSI studies, proved elusive.

243 fatty acid-binding protein, LPS, and soluble LPS receptor soluble CD14 (sCD14).

244 more clinically-relevant E.coli (non-sterile LPS) murine ALI model.

245 We found that miR-145a could suppress LPS-induced NF-kappaB activation.

246 his microcrystal-free preparation suppressed LPS- or MSU crystal-induced monocyte activation, a proce

247 Taken together, C/EBPgamma suppresses LPS- and IgG immune complexes-induced pro-inflammatory m

248 Here, we show that D-mannose suppresses LPS-induced macrophage activation by impairing IL-1beta

249 In vitro data indicated that LPS stimulation evoked a time-dependent increase of HDAC

250 More specifically, we observed that LPS potently stimulated GFAT2 isoform mRNA and protein e

251 We further show that LPS treatment induces Socs1 m(6)A methylation and sustai

252 sed brain to acute stressors, we showed that LPS (100 ug/kg) produced acute cognitive dysfunction, se

253 rrow-derived macrophages (BMDMs) showed that LPS treatment induced a sustained increase in NF-kappaB

254 The LPS + PM group showed increased BALF leukocytes, charact

255 The LPS of Gram-negative bacteria have been shown to activat

256 The LPS-induced drop in blood pressure was higher in SHR tha

257 The LPS-induced serum levels of IL-1beta, TNF-alpha, and IL-

258 regulation in human monocytes attenuated the LPS-induced phosphorylation of IFN regulatory factor 3 a

259 ation but not TAC or PS alone attenuated the LPS-induced pro-inflammatory effects reducing cells and

260 then transported to the cell surface by the LPS transport (Lpt) machinery.

261 DUSP11 deficiency enhanced the LPS-induced TAK1 phosphorylation and cytokine production

262 TNF-alpha plays a pivotal role in the LPS-upregulated astrocyte activation and proliferation,

263 Mutants lacking glucose I of the LPS outer core failed to propagate LL12.

264 Interestingly, SCM potentiated the LPS-induced expression of IL1alpha, IL1beta, and IL6.

265 oinositide 3-kinase inhibitor, prevented the LPS-mediated decrease, demonstrating the role of TLR4-PI

266 e investigated the mechanisms regulating the LPS-induced alternative pre-mRNA splicing of the MyD88 t

267 nd found no evidence for either, making this LPS-to-Lipid A-MSI (LLA-MSI) method, compatible with sim

268 mice reveal an increased sensitivity also to LPS of Escherichia coli, which had no effect in WT mice.

269 ic PbgA-derived peptides selectively bind to LPS in vitro and inhibit the growth of diverse Gram-nega

270 we demonstrate that hGBP1 binds directly to LPS and induces "detergent-like" LPS clustering through

271 enetic alterations, while exposure either to LPS or NNK/LPS in combination led to increased levels of

272 th human and murine myeloid cells exposed to LPS as well as other TLR ligands and inflammatory cytoki

273 els animals were treated with recAP prior to LPS administration.

274 ression of inflammatory genes in response to LPS and other bacterial ligands.

275 dampening the early inflammatory response to LPS by regulating macrophage function, suggesting an ess

276 uding microbial infection and in response to LPS in myeloid and epithelial cells.

277 did not upregulate glycolysis in response to LPS, irrespective of LKB1 presence.

278 Western blotting to show that in response to LPS, LPCAT2, but not LPCAT1, rapidly associates with TLR

279 er in skeletal muscle of mice in response to LPS-induced inflammation.

280 tein secretion in macrophages in response to LPS.

281 e signaling pathways, and in the response to LPS.

282 arkedly attenuated inflammatory responses to LPS challenge.

283 indirectly influence neutrophil responses to LPS.

284 SP11-deficient mice were more susceptible to LPS-induced endotoxic shock.

285 hange in markers of microbial translocation (LPS, IFABP, sCD14, and T-cell activation), with decrease

286 y, modulating the inflammatory response upon LPS stimulation.

287 ammatory responses both in vivo and in vitro LPS stimulates Toll-like receptor 4, an important mediat

288 In vitro, LPS-stimulated migratory TNFRp55(-/-) DCs of MLN increas

289 of a pseudaminic acid derivative, but whose LPS electrophoretic profile was indistinguishable from t

290 When activated with LPS, CF macrophage expressed reduced ferroportin (Fpn).

291 Interestingly, we find that a challenge with LPS treatment significantly increased expression levels

292 days for 3 or 8 weeks, then challenged with LPS (5 mg/kg; IP).

293 microosmotic pumps and were challenged with LPS or underwent cecal ligation and puncture.

294 ro, when added alone, or in combination with LPS or TNF-alpha in ASM.

295 in dams that received LPS DDI compared with LPS SPI.

296 that stimulation of murine macrophages with LPS or DTT facilitated cell surface translocation of cal

297 primary human endothelial cells primed with LPS followed by histamine.

298 Unless previously stimulated with LPS, CCL2 did not cause migration of macrophages.

299 were rapidly induced after stimulation with LPS; however, IL1B mRNA production was less inhibitable

300 lls from the brains of the mice treated with LPS at different time points, and RNA-seq was performed