ライフサイエンスコーパス: lipopolysaccharide

1 bacterial infection (Listeria monocytogenes, lipopolysaccharide).

2 ple, hypotension, hemorrhage and presence of lipopolysaccharides).

3 g receptor expressed on myeloid cells 1) and lipopolysaccharide.

4 cultured both in the presence and absence of lipopolysaccharide.

5 y defined immunostimulatory ligands, such as lipopolysaccharide.

6 stly increased in response to challenge with lipopolysaccharide.

7 nhibits macrophage activation in response to lipopolysaccharide.

8 mponents like bovine serum albumin (BSA) and lipopolysaccharide.

9 lla pneumoniae, Streptococcus pneumoniae, or lipopolysaccharide.

10 responses in human monocytes stimulated with lipopolysaccharide.

11 ling and hypersensitivity to the TLR4 ligand lipopolysaccharide.

12 oglial cells and in HIV-Tg rats administered lipopolysaccharide.

13 IFNgamma) or a combination of bdIFNgamma and lipopolysaccharide.

14 ationic protein and histamine in response to Lipopolysaccharides.

15 ipid A, the hydrophobic portion of bacterial lipopolysaccharides.

16 posure to ionizing radiation or to bacterial lipopolysaccharides.

17 pared with controls (mitochondrial-64 +/- 6, lipopolysaccharide-54 +/- 8, control-14 +/- 1.5, P= 0.00

18 helium, thus preventing the translocation of lipopolysaccharide, a cell wall component of Gram-negati

19 bsence of NOM (including those incorporating lipopolysaccharide, a major bacterial outer membrane com

20 ivation of TLR4 by Gram-negative bacteria or lipopolysaccharide accelerates CCM formation, and geneti

21 less-severe forms of colitis and had reduced lipopolysaccharide activation of the toll-like receptor

22 w that a systemic inflammatory challenge via lipopolysaccharide administration potently enhances seiz

23 A) monocytes in response to stimulation with lipopolysaccharide also is dependent on the caspase-1-AS

24 ere consistent with stimulation by bacterial lipopolysaccharide; an influx of macrophages and appeara

25 Nlrp3 activation induced by incubation with lipopolysaccharide and ATP was studied in vitro in norma

26 at 2 hours postchallenge during the peaks of lipopolysaccharide and bacteremia but not of TAT and PAP

27 munomodulatory macromolecules-peptidoglycan, lipopolysaccharide and capsular polysaccharide-either si

28 two mouse models of sepsis-intra-peritoneal lipopolysaccharide and cecal ligation and puncture.

29 tagenome characterized by elevated levels of lipopolysaccharide and flagellin.

30 at GSDMD plays a critical role in regulating lipopolysaccharide and NLRP3-mediated interleukin-1beta

31 ernating lateral access mechanism to extract lipopolysaccharide and traffic it along the hydrophobic

32 Mice were injected with lipopolysaccharide and/or aldosterone.

33 ate pathway, and others predicted to mediate lipopolysaccharides and cell wall modification.

34 It is unknown if LPS (lipopolysaccharides) and markers of immune activation, s

35 6 weeks, and analyzed for lipids, cytokines, lipopolysaccharide, and insulin.

36 Serum levels of bacterial lipopolysaccharide are raised in T2D, and we recently sh

37 monary innate immune response to bacteria or lipopolysaccharide, as assessed by neutrophil recruitmen

38 at a mutant version of a protein involved in lipopolysaccharide assembly, lptD4213, is synthetically

39 acrophages were isolated and stimulated with lipopolysaccharide, ATP, or both.

40 rats, controls the innate immune response to lipopolysaccharide attenuating the plasma levels of infl

41 flammatory and anti-inflammatory markers and lipopolysaccharide binding protein (LBP) plasma as well

42 trations of HDL-bound serum amyloid A (SAA), lipopolysaccharide binding protein (LBP), apolipoprotein

43 Complement C5A anaphylatoxin (C5A), lipopolysaccharide binding protein (LBP), C-reactive pro

44 Subgroup analyses on patients with increased lipopolysaccharide binding protein and systemic vascular

45 as measured by soluble CD14, soluble CD163, lipopolysaccharide binding protein, and microbial 16s ri

46 ration rate and plasma renin, noradrenaline, lipopolysaccharide binding protein, troponin T, and brai

47 dicated by the regularisation of clotting by lipopolysaccharide-binding protein (LBP).

48 trations of gut-derived hormones, incretins, lipopolysaccharide-binding protein, or other markers of

49 nistration of saline, lipopolysaccharide, or lipopolysaccharide + blocking showed a 3.2-fold increase

50 nistration of saline, lipopolysaccharide, or lipopolysaccharide + blocking, and 2-compartment, 5-para

51 in-2 to fungal mannans and also to bacterial lipopolysaccharides, capsular polysaccharides, and lipoa

52 As for flagellin or lipopolysaccharides, CdtB also induced expression of inf

53 defective PMN transmigration in response to lipopolysaccharide challenge in adult mice in which the

54 PAPC against tumor necrosis factor-alpha and lipopolysaccharide challenge were suppressed in human pu

55 uced plasma TNFalpha in response to systemic lipopolysaccharide challenge, together suggesting that t

56 o monocyte chemotactic protein 1 (MCP-1) and lipopolysaccharide compared with WT mouse macrophages.

57 ospholipids comprising the inner leaflet and lipopolysaccharides comprising the outer leaflet (1-3) .

58 tective efficacy of broad-ranging Salmonella lipopolysaccharide conjugate vaccines.

59 egative organisms due to the presence of the lipopolysaccharide-containing outer membrane, which acts

60 Lipopolysaccharide dispersed in the blood by Gram-negati

61 t mice exhibit increased sensitivity to high lipopolysaccharide doses.

62 ary in vitro studies, NDP-MSH attenuated the lipopolysaccharide elicited apoptosis, hypermotility and

63 However, priming with lipopolysaccharide, followed by stimulation with ATP, le

64 Stimulating Mregs with 100 ng/mL lipopolysaccharide for 24 hours did not extinguish DHRS9

65 usion channels were stimulated with 1 mug/mL lipopolysaccharide for 6 hours and perfused with 100 mum

66 ng cassette transporters because it extracts lipopolysaccharide from the external leaflet of the inne

67 -dependent (concanavalin A) and independent (lipopolysaccharide/galactosamine) hepatitis and in model

68 We report that lipopolysaccharide/galactosamine-induced liver injury de

69 ndrial product (204 +/- 12 and 41 +/- 1) and lipopolysaccharide groups (178 +/- 18 and 42 +/- 0.5) co

70 injection in the mitochondrial products and lipopolysaccharide groups compared with controls (170 +/

71 was significantly worse in mitochondrial and lipopolysaccharide groups compared with controls (mitoch

72 was stimulated with Escherichia coli derived lipopolysaccharide, heat-killed Streptococcus pneumoniae

73 Peripheral anti-lipopolysaccharide immunoglobulin G and immunoglobulin A

74 function is distinct from that triggered by lipopolysaccharide in both its broad effects on multiple

75 and reduced inflammatory response caused by lipopolysaccharide in macrophages RAW 264.7.

76 ne is a unique asymmetric lipid bilayer with lipopolysaccharide in the outer leaflet.

77 for acute inflammatory responses induced by lipopolysaccharide in vivo; notably, this regulation did

78 To illuminate the roles of both Ca(2+) and lipopolysaccharides in protein functionality, we perform

79 P3 inflammasome or the presence of bacterial lipopolysaccharides in the case of the non-canonical inf

80 Finally, in vivo administration of lipopolysaccharide increased liver injury and the levels

81 Moreover, injection of lipopolysaccharide induced rapid inflammatory gene expre

82 mg kg(-1) i.p.) also significantly improved lipopolysaccharide-induced cognitive deficits.

83 Specifically, we show that IL-10 inhibits lipopolysaccharide-induced glucose uptake and glycolysis

84 Lipopolysaccharide-induced in vitro enteric neurodegener

85 We also determined that cNK-2 suppresses the lipopolysaccharide-induced inflammatory response by abro

86 or-alpha in vitro and in the animal model of lipopolysaccharide-induced lung injury.

87 , or Rac1-deficient mice were protected from lipopolysaccharide-induced lung injury.

88 stinal fatty acid binding protein [I-FABP]), lipopolysaccharide-induced monocyte activation (soluble

89 microglia-mediated inflammation in an acute lipopolysaccharide-induced neuro-inflammation model in m

90 SHISA2 expression, which are involved in the lipopolysaccharide-induced platelet-derived growth facto

91 se-2 and interleukin-8 mRNA expression after lipopolysaccharide induction in CaCo-2, showing an anti-

92 Lack of CD47 also limits lipopolysaccharide induction of IL-1beta, NLRP3, and cas

93 ritonitis and 22 pigs that were subjected to lipopolysaccharide infusion.

94 diac dysfunction" induced by intraperitoneal lipopolysaccharide injection (10 mg/kg), hemodynamic eff

95 , we challenged male Wistar rats to repeated lipopolysaccharide instillations, associated or not with

96 quently translocation of bacterial endotoxin-lipopolysaccharide into the blood.

97 nds across the periplasm to directly deliver lipopolysaccharide into the external leaflet of the oute

98 The lipopolysaccharide is a virulence factor of this pathoge

99 The O-antigen side chain of the lipopolysaccharide is an immunodominant antigen, can def

100 The lipid A domain of the endotoxic lipopolysaccharide layer of Gram-negative bacteria is co

101 High levels of lipopolysaccharide lead to apoptosis in cultured myenter

102 t activation of dendritic cells by bacterial lipopolysaccharide leads to increased FRET of fluorescen

103 were stimulated with purified Aa serotype b lipopolysaccharide (LPS) (Aa-LPS), heat-killed (HK) bact

104 enon, termed "inducible renitence," in which lipopolysaccharide (LPS) activation of macrophages prote

105 rophil subsets or reflect changes induced by lipopolysaccharide (LPS) activation.

106 buminuric type 1 diabetes patients with high lipopolysaccharide (LPS) activity, known to predict prog

107 The present study assessed the effect of lipopolysaccharide (LPS) administration at a dose of 2 n

108 In the current study, we examined whether lipopolysaccharide (LPS) administration decreased autoph

109 e tested whether bacterial endotoxin E. coli lipopolysaccharide (LPS) affected two dissociable constr

110 protective effect on D-galactosamine (GaIN)/lipopolysaccharide (LPS) and concanavalin A (ConA)-induc

111 were cultured with Porphyromonas gingivalis lipopolysaccharide (LPS) and cytosine-phospho-guanine (C

112 amyloid-like aggregates with both bacterial lipopolysaccharide (LPS) and gram-negative bacteria.

113 ocation, characterized by elevated levels of lipopolysaccharide (LPS) and related markers, is a commo

114 l-like receptor (TLR) agonism with bacterial lipopolysaccharide (LPS) and the synthetic acylated lipo

115 olated blood leukocytes exposed to bacterial lipopolysaccharide (LPS) as well as in vivo following LP

116 sed survival against a septic challenge with lipopolysaccharide (LPS) by 2-fold.

117 ed macrophages, tPA inhibits the response to lipopolysaccharide (LPS) by a pathway that apparently re

118 An elevated plasma concentration of lipopolysaccharide (LPS) caused by increased intestinal

119 e-mimetic anionic surfactant as well as with lipopolysaccharide (LPS) constituting the outer leaflet

120 Lipopolysaccharide (LPS) decreased food/water intake and

121 The observation that high doses of Lipopolysaccharide (LPS) drove rapid monocyte differenti

122 Lipopolysaccharide (LPS) extracted from mcr-1 strains in

123 ments and tested by sensor measurements with lipopolysaccharide (LPS) from E. coli B, E. coli 056, E.

124 alteration in the lipid A composition of its lipopolysaccharide (LPS) from the penta-acylated (PgLPS1

125 ats challenged with a high dose of bacterial lipopolysaccharide (LPS) in a thermogradient apparatus.

126 A high-fat diet increases bacterial lipopolysaccharide (LPS) in the circulation and thereby

127 OM) of Gram-negative bacteria is composed of lipopolysaccharide (LPS) in the outer leaflet and phosph

128 Lipopolysaccharide (LPS) in the outer membrane of Gram-n

129 24 h and then subjected to stimulation with lipopolysaccharide (LPS) in the presence or absence of M

130 induced with intratracheal administration of lipopolysaccharide (LPS) in wild-type (n = 19) and CCR2-

131 Activation of TLR4 by lipopolysaccharide (LPS) induces both pro-inflammatory a

132 In particular, lipopolysaccharide (LPS) induces expression of MsrB1, bu

133 of Toll-like receptor 4 (TLR4) by bacterial lipopolysaccharide (LPS) initiates inflammation and prom

134 Gram-negative bacterial endotoxin lipopolysaccharide (LPS) is implicated in acute and chro

135 Systemic lipopolysaccharide (LPS) is implicated in increasing mor

136 We investigated if bacterial lipopolysaccharide (LPS) is implicated in platelet activ

137 Lipopolysaccharide (LPS) is the component of Gram-negati

138 crobiota dysbiosis was investigated by fecal lipopolysaccharide (LPS) measurement and metabolomics (l

139 of VLX103 in the d-galactosamine (GalN) and lipopolysaccharide (LPS) model of acute, fulminant liver

140 t RcsF monitors lateral interactions between lipopolysaccharide (LPS) molecules.

141 ities with the bifunctional Escherichia coli lipopolysaccharide (LPS) O antigen regulator WbdD.

142 a tetrasaccharide from the O-antigen of the lipopolysaccharide (LPS) of Francisella tularensis bacte

143 (TLR-4), a protein responsible for detecting lipopolysaccharide (LPS) of Gram-negative bacteria, was

144 This asymmetry, with lipopolysaccharide (LPS) or lipooligosaccharide (LOS) ex

145 (KO) mice, with neuroinflammation induced by lipopolysaccharide (LPS) or oAbeta.

146 ived unilateral intranasal administration of lipopolysaccharide (LPS) or saline three times per week,

147 Lipopolysaccharide (LPS) or vehicle was administered per

148 IFN-gamma or lipopolysaccharide (LPS) polarizes macrophages toward th

149 genesis is affected by overexpression of the lipopolysaccharide (LPS) receptors CD14 and TLR4, which

150 oblast-stimulating lipoprotein 1 [FSL-1]) or lipopolysaccharide (LPS) significantly induced proinflam

151 , ex vivo blood tests on immunoreactivity to lipopolysaccharide (LPS) stimulation, and cognitive func

152 tes exhibited reduced cytokine release after lipopolysaccharide (LPS) stimulation, and CTSD KO also r

153 Here, we demonstrate that upon lipopolysaccharide (LPS) stimulation, macrophages shift

154 d that in response to bacterial infection or lipopolysaccharide (LPS) stimulation, macrophages upregu

155 Lipopolysaccharide (LPS) surface charge and aggregation

156 Eagan strains expressing well-characterized lipopolysaccharide (LPS) surface structures of various l

157 3 priming in vivo involved administration of lipopolysaccharide (LPS) to HIV transgenic (Tg) rats fol

158 uman primary macrophages were incubated with lipopolysaccharide (LPS) to induce expression of NLRP3,

159 hibitor trichostatin A blocks the ability of lipopolysaccharide (LPS) to suppress Rgs10 transcription

160 Lipid A anchors the lipopolysaccharide (LPS) to the outer membrane and is us

161 to alter gyrase, but the ATPase that powers lipopolysaccharide (LPS) transport.

162 etylate FOXO3 in vitro and in vivo, and that lipopolysaccharide (LPS) treatment of THP-1 monocytes in

163 Increasing demand for myeloid cells via lipopolysaccharide (LPS) treatment specifically recruits

164 is deleted in myeloid cells, the response to lipopolysaccharide (LPS) was greatly exacerbated.

165 thrombin in endothelial cells in response to lipopolysaccharide (LPS) with or without pretreatment of

166 a salt that creates gastric discomfort, and lipopolysaccharide (LPS), a bacterial cell wall componen

167 ration of compounds that block the action of lipopolysaccharide (LPS), a constituent of the Gram-nega

168 d in leukocytes and neutrophils treated with lipopolysaccharide (LPS), a ligand of TLR4, in vitro.

169 mmatory response induced by Escherichia coli lipopolysaccharide (LPS), a Toll-like receptor (TLR)-4 a

170 ol 12-myristate 13-acetate/ionomycin (PI) or lipopolysaccharide (LPS), and stained for Tregs (CD4(+)

171 microbial peptides through aminoacylation of lipopolysaccharide (LPS), expected to decrease the negat

172 with the toll-like receptor (TLR)-4 ligand, lipopolysaccharide (LPS), in the presence and absence of

173 l lipid A (MPLA), a less toxic derivative of lipopolysaccharide (LPS), is employed as a vaccine adjuv

174 ated) T-cell frequency, and plasma levels of lipopolysaccharide (LPS), LPS binding protein (LBP), sol

175 Due to the high toxicity of bacterial lipopolysaccharide (LPS), resulting in sepsis and septic

176 Following IP injection of lipopolysaccharide (LPS), serum levels of IL1beta and TN

177 e set of eukaryotic receptors that recognize lipopolysaccharide (LPS), the major outer-membrane compo

178 on the cell surface of murine neutrophils by lipopolysaccharide (LPS), tumor necrosis factor, and zym

179 Here, focusing on macrophage responses to lipopolysaccharide (LPS), we use the hybrid mouse divers

180 programming of neuroinflammation induced by lipopolysaccharide (LPS), we validated this hypothesis i

181 onstrate that cholangiocytes stimulated with lipopolysaccharide (LPS), which is a membrane component

182 he offspring also received a second 'hit' of lipopolysaccharide (LPS), which simulates a bacterial in

183 mal effects on B cell responses activated by lipopolysaccharide (LPS), which stimulates B cells in an

184 prototype vaccine formulation consisting of lipopolysaccharide (LPS)-detoxified outer membrane vesic

185 Lipopolysaccharide (LPS)-induced expression of IFN-beta

186 was measured by a DNA-binding assay, and ii) lipopolysaccharide (LPS)-induced human monocyte release

187 During the resolving phase of lipopolysaccharide (LPS)-induced inflammation when resol

188 ls against H2O2-induced oxidative stress and lipopolysaccharide (LPS)-induced inflammation, at low co

189 tudies indicated that chrysophanol inhibited lipopolysaccharide (LPS)-induced iNOS and COX-2 expressi

190 HMGB1 signaling cascade and inflammation in lipopolysaccharide (LPS)-induced keratinocytes and imiqu

191 Recent studies demonstrate that in mice lipopolysaccharide (LPS)-induced lethality is prevented

192 ion and bone resorption in a murine model of lipopolysaccharide (LPS)-induced periodontal disease.

193 ion and bone resorption in a murine model of lipopolysaccharide (LPS)-induced periodontal disease.

194 tion of protein tyrosine phosphatase Shp2 to lipopolysaccharide (LPS)-induced renal injury.

195 identify a therapeutic function for hRetn in lipopolysaccharide (LPS)-induced septic shock.

196 expression and glucocorticoid sensitivity in lipopolysaccharide (LPS)-induced sudden sensorineural he

197 ained oral and ocular efficacy in a model of lipopolysaccharide (LPS)-induced systemic AP activation

198 signaling cascades (NF-kappaB and MAPKs) in lipopolysaccharide (LPS)-stimulated macrophages.

199 nificant anti-inflammatory effects, reducing lipopolysaccharide (LPS)-stimulated ROS, nitric oxide an

200 roduced higher levels of IL-8 and CCL-2 upon lipopolysaccharide (LPS)-stimulation.

201 Alcohol disrupted lipopolysaccharide (LPS)-TLR4-ERK1/2-cyclin D1 signaling

202 n the CNS after peripheral administration of lipopolysaccharide (LPS).

203 upon exposure to bacterial products, such as lipopolysaccharide (LPS).

204 dels of liver injury and strongly induced by lipopolysaccharide (LPS).

205 d by proinflammatory cytokines and bacterial lipopolysaccharide (LPS).

206 maturation upon TLR4 activation by ultrapure lipopolysaccharide (LPS).

207 logenetic expectations to add amino acids to lipopolysaccharide (LPS).

208 1 and caspase-11 upon detection of cytosolic lipopolysaccharide (LPS).

209 n macrophages activated with the TLR4 ligand lipopolysaccharide (LPS).

210 es does not prevent induction of hepcidin by lipopolysaccharide (LPS).

211 ntrolling bacterial surface features such as lipopolysaccharide (LPS).

212 1, an enzyme that binds oxPAPC and bacterial lipopolysaccharide (LPS).

213 thrombin and proinflammatory bacterial wall lipopolysaccharide (LPS).

214 pact of 6 weeks of ethanol diet and/or acute lipopolysaccharide (LPS).

215 ice with paw inflammation that is induced by lipopolysaccharide (LPS).

216 ex) treatment before or after stimulation by lipopolysaccharide (LPS).

217 ently activated with an endotoxin injection [lipopolysaccharide (LPS)].

218 t of rats received intravenous injections of lipopolysaccharide (LPS, 3 mg/kg per week) to induce pan

219 inal disease, colitis-associated cancer, and lipopolysaccharide (LPS, the main component of G(-) bact

220 Firmicutes, but possess outer membranes with lipopolysaccharide (LPS-OM).

221 n this study, we investigated the effects of lipopolysaccharides (LPS) and interleukin (IL)-17A on th

222 Lipopolysaccharides (LPS) are essential outer membrane g

223 toward the transporter's periplasmic domains.Lipopolysaccharides (LPS) are synthesized at the peripla

224 have highlighted the importance of Bp and Bm lipopolysaccharides (LPS) as vaccine candidates.

225 d small-angle X-ray scattering, we show that lipopolysaccharides (LPS) form bilayers that interact wi

226 ifferent methods of CS exposure, plus airway Lipopolysaccharides (LPS) inhalation, in building our CO

227 s rat fecal Gram-negative bacteria, elevates lipopolysaccharides (LPS), and induces intestinal pathol

228 lly regulated by a proinflammatory stimulus (lipopolysaccharide [LPS] from Porphyromonas gingivalis)

229 onents were released in mouse models of both lipopolysaccharide(LPS)-induced shock (LPSS) and hemorrh

230 pea protein hydrolysate (PPH) by attenuating lipopolysaccharide- (LPS) induced pro-inflammatory gene

231 Lipopolysaccharides (LPSs) are a major component of the

232 g secretion systems, putative effectors, and lipopolysaccharides (LPSs), as well as other important t

233 M2.5-bound trace microbial elements, such as lipopolysaccharide may be a strong candidate for exacerb

234 BTKB66 potently inhibited lipopolysaccharide-mediated activation of bone marrow-de

235 rst, BTKB66 was tested in in vitro models of lipopolysaccharide-mediated neutrophil and macrophage ac

236 In the lipopolysaccharide model of inflammation, RVX-297 reduce

237 In the intratracheal lipopolysaccharide model, 1,500 IU of intraperitoneal ch

238 pe semiconductors and they can interact with lipopolysaccharide molecules present in the outer membra

239 f lung injury induced by bacterial products (lipopolysaccharide n = 5).

240 with antibacterial, receptor-activating, and lipopolysaccharide-neutralizing abilities of these chemo

241 the importance of the AcrAB efflux pump and lipopolysaccharide O-antigen synthesis for bile salt res

242 to peptidoglycan, N-linked glycoproteins and lipopolysaccharide O-antigen.

243 ncreased prevalence of Klebsiella pneumoniae lipopolysaccharide O2 serotype strains in all major drug

244 relies on sensing the cytosolic presence of lipopolysaccharide of Gram-negative bacteria via inflamm

245 inkage in the polylegionaminic acid from the lipopolysaccharide of the Legionella pneumophila virulen

246 hat monocytes activated by interferon alpha, lipopolysaccharide or a combination of both generate exo

247 Lipopolysaccharide or ATP stimulation alone did not acti

248 Upon lipopolysaccharide or cecal ligation and puncture-induce

249 Mice were treated with lipopolysaccharide or hydrochloric acid.

250 We demonstrated that the addition of lipopolysaccharide or peptidoglycan of bacterial origin

251 ubjects (n = 16) were stimulated with either lipopolysaccharide or phytohemagglutinin.

252 inhibition of tumour necrosis factor (TNF), lipopolysaccharide or polyinosinic:polycytidylic acid (p

253 TLR4 stimulation with lipopolysaccharides or live bacteria enhanced tumorigene

254 knockout mice were injected with endotoxin (lipopolysaccharide) or fed a methionine and choline-defi

255 mice at 72 h after administration of saline, lipopolysaccharide, or lipopolysaccharide + blocking sho

256 mice at 72 h after administration of saline, lipopolysaccharide, or lipopolysaccharide + blocking, an

257 In mice, lipopolysaccharide- or Escherichia coli-induced peritoni

258 strate, including the polyketide sugar unit, lipopolysaccharide, peptidoglycan and terpenoid backbone

259 utively released or Porphyromonas gingivalis lipopolysaccharide (PgLPS)-stimulated epithelial superna

260 lation of the IAP substrate and TLR4 ligand, lipopolysaccharide-phosphate.

261 a series of oligosaccharides that mimic the lipopolysaccharides present on the pathogens' surface an

262 ng the second week by treatment with PGE2 or lipopolysaccharides produces enduring consequences as a

263 sitivity to osmotic and detergent stress and lipopolysaccharide profile and an increased ability to i

264 Herein, we found that the bacterial lipopolysaccharide receptor CD14 captured extracellular

265 At baseline, CXCL10, lipopolysaccharide, soluble CD14, 16S ribosomal DNA, and

266 In lipopolysaccharide-stimulated human THP1 monocytes, ARID

267 Secretion of interleukin 6 (IL-6) in lipopolysaccharide-stimulated monocytes was used as a pr

268 ne questionnaire, interview, and blood draw (lipopolysaccharide-stimulated production of interleukin

269 r effects on nitric oxide (NO) production in lipopolysaccharide-stimulated RAW264.7 macrophages.

270 ed importin alpha5 expression and normalized lipopolysaccharide-stimulated tumor necrosis factor alph

271 asal and platelet-activating factor (PAF) or lipopolysaccharide-stimulated vascular leakage compared

272 Peripheral monocyte response to lipopolysaccharide stimulation was lower in alcohol-depe

273 D who had a proinflammatory profile based on lipopolysaccharide stimulation were more developmentally

274 leukocyte cytokine secretion in response to lipopolysaccharide stimulation.

275 face of most Gram-negative bacteria contains lipopolysaccharide that is essential for their viability

276 ty to incorporate exogenous fatty acids, and lipopolysaccharides that are not essential.

277 We show that treatment of B cells with lipopolysaccharide, the ligand for TLR4, results in SYK

278 In the case of lipopolysaccharide, this is a delayed, Toll/interleukin-

279 etect bacterial toxins, formyl peptides, and lipopolysaccharides through distinct molecular mechanism

280 Of note, D-RR4 was able to bind to lipopolysaccharide to reduce the endotoxin-induced proin

281 s, V. cholerae O-specific polysaccharide and lipopolysaccharide, toxin coregulated pilus A, sialidase

282 Here we report the crystal structure of the lipopolysaccharide transporter LptB2FG from Klebsiella p

283 stern blot analysis of P2X7R for saline- and lipopolysaccharide-treated brain sections showed a respe

284 ibution studies were performed on saline- or lipopolysaccharide-treated mice at 15, 30, and 60 min af

285 tribution of (11)C-GSK1482160 in saline- and lipopolysaccharide-treated mice at 72 h was statisticall

286 Whole-brain Iba1 expression in lipopolysaccharide-treated mice peaked by 72 h on immuno

287 s by preventing cell death in both naive and lipopolysaccharide-treated mixed glia.

288 Peak immune response to lipopolysaccharide treatment in mice was determined in t

289 xhibit higher innate immune reactivity after lipopolysaccharide treatment.

290 astrocytes by the proinflammatory endotoxin lipopolysaccharide via both nuclear factor-kappaB and si

291 At day 10 post burn, 2 mg/kg of lipopolysaccharide was administered IV, and the presence

292 motic and detergent stress, lacked very long lipopolysaccharide, was unable to invade enterocytes, an

293 ecal ligation and puncture and intratracheal lipopolysaccharide were undertaken in normal and vitamin

294 (Kdo) is an essential component of bacterial lipopolysaccharides, where it provides the linkage betwe

295 ssociated molecular patterns (PAMPs, such as lipopolysaccharides), which leads to premature cell deat

296 owards the inner core tetrasaccharide of the lipopolysaccharide, which were capable of binding the ce

297 Lipopolysaccharide whole-blood stimulation resulted in a

298 o demonstrated that stimulation of TLR4 with lipopolysaccharide, widely used to examine microglial re

299 ivation in response to the bacterial product lipopolysaccharide with concomitant impairment in the pr

300 th on the signaling cascade initiated by the lipopolysaccharide with the glycerophosphoinositol-depen