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1  inflamed by intratracheal administration of lipopolysaccharide.
2 essive phenotype when challenged in vitro by lipopolysaccharide.
3 d by the Toll-like receptor 4 (TLR4) agonist lipopolysaccharide.
4 upon stimulation with the pathogen component lipopolysaccharide.
5 vation, nutrient deprivation, rapamycin, and lipopolysaccharide.
6  component is likely to be the extracellular lipopolysaccharide.
7 ty in mice after exposure to toxic levels of lipopolysaccharide.
8 ers the metabolism of macrophages exposed to lipopolysaccharide.
9 elated stimulus, including live pathogens or lipopolysaccharide.
10 e bacterium E. coli, CLP, or E. coli derived lipopolysaccharide.
11 soluble IL7R (sIL7R) are markedly induced by lipopolysaccharide.
12  produced by lipid A, the membrane anchor of lipopolysaccharide.
13 bacteria, S-layers are anchored to cells via lipopolysaccharide.
14 crescentus S-layer bound to the O-antigen of lipopolysaccharide.
15 , angiotensin II, aldosterone, cisplatin and lipopolysaccharide.
16 Wzt ABC transporter for ligation to the core lipopolysaccharides.
17 sponse to acute neuroinflammation induced by lipopolysaccharides.
18  innate immune system by sialylating surface lipopolysaccharides.
19 Toll-like receptor 4 (TLR4)/MyD88 sensing of lipopolysaccharides.
20 he outer membrane are due to the presence of lipopolysaccharide(1).
21  by a single intratracheal administration of lipopolysaccharide (10, 20, or 40 mug per mouse) in C57B
22              C57BL/6J mice were administered lipopolysaccharide (15 mg/kg) or saline (vehicle) and se
23 with either live microbes or microbe-derived lipopolysaccharides (a ligand for TLR4), macrophages wit
24  the lung, a first event, and followed by IV lipopolysaccharide, a second event, resulted in ARDS in
25 , we assembled a functional cis-regulome for lipopolysaccharide-activated B cells.
26 ta, as well as the inflammatory responses to lipopolysaccharide and dexamethasone were unchanged.
27  macrophages, generated by polarization with lipopolysaccharide and interferon-gamma, showed signific
28 lated in human myeloid cells stimulated with lipopolysaccharide and other innate immune stimuli.
29         Furthermore, metformin reduces blood lipopolysaccharides and its initiated low-grade inflamma
30 arn operon, mediating arabinosaminylation of lipopolysaccharides and related regulatory systems, was
31 me ventilation against lung injury caused by lipopolysaccharides and ventilation at high tidal volume
32 crosis factor alpha], IL-1alpha) and in vivo lipopolysaccharide- and atherogenic diet-induced NF-kapp
33 and uncover how the capture and extrusion of lipopolysaccharide are coupled to conformational rearran
34                                              Lipopolysaccharides are anchored to the outer membrane o
35                                              Lipopolysaccharides are critical components of bacterial
36 orming group A colicin N (ColN) instead uses lipopolysaccharide as a receptor.
37 levels were quantified following exposure to lipopolysaccharide as an inflammatory stimulus.
38 ength of the O-antigen on cells and show how lipopolysaccharide binding and S-layer assembly is regul
39 inal fatty acid binding protein (I-FABP) and lipopolysaccharide binding protein (LBP) did not differ
40 els of APPs, including soluble CD14 (sCD14), lipopolysaccharide binding protein (LBP), and C-reactive
41 actors, and the CD4/CD8 T-cell ratio, higher lipopolysaccharide-binding protein (LBP) was associated
42 ctive protein (CRP), Procalcitonin (PCT) and Lipopolysaccharide-binding protein (LBP).
43 ed with higher systolic blood pressure, TGs, lipopolysaccharide-binding protein, and lower HDL choles
44              Chemokine (C-C motif) ligand 2, lipopolysaccharide-binding protein, C-reactive protein,
45                                          The lipopolysaccharide biosynthesis pathway is considered an
46 cyltransferase LpxA, the first enzyme in the lipopolysaccharide biosynthesis pathway.
47                                    Genes for lipopolysaccharide biosynthesis were enriched in microbi
48  family 25, whose activities are exclusively lipopolysaccharide biosynthesis.
49 naling upon innate immune recognition of the lipopolysaccharide biosynthetic intermediate beta-ADP-he
50  angiotensin II, high glucose, cisplatin and lipopolysaccharide, but was induced by aristolochic acid
51 ages safeguards mice from lethal exposure to lipopolysaccharides, but this protection is not conferre
52                                        While lipopolysaccharide causes nuclear-cytoplasmic translocat
53 ET studies were included: before and after a lipopolysaccharide challenge (8 subjects), in alcohol us
54 nhibition of IRAK-1/4 or TAK1 in response to lipopolysaccharide challenge in human rheumatoid arthrit
55  cultured primary astrocytes stimulated with lipopolysaccharide, conditioned media from mesenchymal s
56 scle cell interactions under high glucose or lipopolysaccharide conditions.
57 ined intestinal barrier function and reduced lipopolysaccharides content in blood, thereby helping to
58  containing TIMP-GLIA, anti-CD3 antibody, or lipopolysaccharide (controls) and analyzed in proliferat
59 rtion sequences or mutations in O-antigen or lipopolysaccharide core biosynthesis genes, affecting th
60 f Ctsk (-/-) dendritic cells stimulated with lipopolysaccharide demonstrated that the ablation of Cts
61  phenotype could be potentiated inducing the lipopolysaccharide depression model.
62                                              Lipopolysaccharide derived from Gram-negative bacteria i
63 nd their controls, and the administration of lipopolysaccharide did not change V(ND) Conclusion: Our
64   There was a strong correlation between the lipopolysaccharide dose and (64)Cu-LLP2A uptake, as quan
65 lpha (TNF-alpha), IL-1beta, Escherichia coli lipopolysaccharide (Ec-LPS) and Porphyromonas gingivalis
66                                 We find that lipopolysaccharide elicits gasdermin D-dependent pyropto
67  (environmental enrichment) and detrimental (lipopolysaccharide from Escherichia coli) stimuli.SIGNIF
68 o-membrane bridge that mediates transport of lipopolysaccharide from the inner membrane to the cell s
69 sults show that, on chronic stimulation with lipopolysaccharides, glutamatergic, but not GABAergic, n
70 hat, during the activation of macrophages by lipopolysaccharides, HDAC3 is recruited to activating tr
71 bjects among whom eight were challenged with lipopolysaccharide in a clinically controlled setting (h
72  elevated insulin and gut-microbiome-derived lipopolysaccharide in response to feeding are required f
73  Conversely, hepcidin was still increased by lipopolysaccharide in Smad158;Alb-Cre(+) mice, although
74 model membranes composed of phospholipids or lipopolysaccharides in aqueous environments.
75 ram-negative bacteria where they extend core lipopolysaccharides in the extracellular leaflet of the
76 many of the observed microglial changes upon lipopolysaccharide, including alterations in microglial
77 ow-fed CysC KO mice were more susceptible to lipopolysaccharide-induced adipose tissue inflammation.
78 ifying lung inflammation in a mouse model of lipopolysaccharide-induced ALI.
79 n vitro, this inhibitor protected cells from lipopolysaccharide-induced cell death, inhibiting NO for
80 ts were distributed in groups 1) control, 2) lipopolysaccharide-induced EP (LPS), and 3) LPS plus cap
81 rentiated U937 cells significantly inhibited lipopolysaccharide-induced expression of tumor necrosis
82  a high anti-inflammatory response caused by lipopolysaccharide-induced in RAW 264.7 macrophages.
83 ippocampus and olfactory bulb was reduced by lipopolysaccharide-induced inflammation.
84 tion rates in a mouse model of non-cancerous lipopolysaccharide-induced inflammation.
85                  We previously reported that lipopolysaccharide-induced inflammatory lymphangiogenesi
86 mulation and failed to enhance resolution of lipopolysaccharide-induced lung inflammation.
87      Crth2 receptor signaling down-regulates lipopolysaccharide-induced NF-kappaB activation in murin
88 h two case studies, simplified apoptosis and lipopolysaccharide-induced NFkappaB signaling pathways,
89 fish oil and its inhibitory response against lipopolysaccharide-induced nitric oxide production in ra
90  mediator, was specifically ubiquitinated in lipopolysaccharide-induced pro-inflammatory macrophages,
91 chievable in the lung (100 uM) inhibited the lipopolysaccharide-induced release of TNF-a (by 76%), IL
92 pyroptosis and cytokine release in cells and lipopolysaccharide-induced septic death in mice.
93     The result obtained demonstrate that, in lipopolysaccharide-induced SI, an increased hypothermia
94 bsence of MK2-mediated necrosome activation, lipopolysaccharide-induced TNFalpha expression was drast
95 at modify the QT interval upstream of LITAF (lipopolysaccharide-induced tumor necrosis factor-alpha f
96 otein marker (TM7318) and high expression of lipopolysaccharide-induced tumor necrosis factor-alpha t
97                        Antibiotic treatment, lipopolysaccharide injection to mice, and in vitro exper
98                       Results: Intratracheal lipopolysaccharide instillation led to an acute inflamma
99 bound lipopolysaccharide, reveal transporter-lipopolysaccharide interactions with side-chain details
100 as mimicked by injection of a single dose of lipopolysaccharide into hypercholesterolemic mice.
101 ECLs) in LptD, an essential OMP that inserts lipopolysaccharide into the outer membrane of Escherichi
102                   In Gram-negative bacteria, lipopolysaccharide is essential for outer membrane forma
103                                              Lipopolysaccharide is recognized by receptors on KCs tha
104 l, bypassing the polar barrier formed by the lipopolysaccharide leaflet on the cell surface.
105 hat autophagy blocks mouse liver injury from lipopolysaccharide led to an examination of autophagy's
106 irulence factor capsular polysaccharides and lipopolysaccharides linked to the cell wall.
107 molecular dynamics simulations, we show that lipopolysaccharide lipid length affects OMV shape at the
108 anes, whereas OMVs with shorter (rough-type) lipopolysaccharide lipids distort and spread over the ho
109 ogen interface: OMVs with long (smooth-type) lipopolysaccharide lipids retain their spherical shape w
110             While urine assays to detect the lipopolysaccharide lipoarabinomannan (LAM), present in m
111                       In contrast, microbial lipopolysaccharide, lipoteichoic acid and flagellin stim
112 nd that the internalized bacterial endotoxin lipopolysaccharide (LPS) activated the pore-forming prot
113 d by faster accumulation of glycine-modified lipopolysaccharide (LPS) and depletion of outer membrane
114 d to inflammatory mix (IM), a combination of lipopolysaccharide (LPS) and high mobility group box 1 (
115 tion, indicated by the presence of bacterial lipopolysaccharide (LPS) and LPS control factors such as
116 e by human neutrophil elastase and aggregate lipopolysaccharide (LPS) and the Gram-negative bacterium
117 ), and Zfp36 (-/-) mice with graded doses of lipopolysaccharide (LPS) and various inhibitors to evalu
118 heir interactions with gut-derived bacterial lipopolysaccharide (LPS) are implicated in hepatic fibro
119                          Our data identified lipopolysaccharide (LPS) as a bona fide effector caspase
120 ne expression using Porphyromonas gingivalis lipopolysaccharide (LPS) as a pathogen, 2) a subcutaneou
121 tection, 120 pM) of Escherichia coli O111:B4 lipopolysaccharide (LPS) associated with sepsis shock in
122  ultrasound guided intrauterine injection of lipopolysaccharide (LPS) at E17 stimulates preterm deliv
123 es in M. xanthus implicated in O-antigen and lipopolysaccharide (LPS) biosynthesis and examined the r
124 terial virulence factor lipid A derived from lipopolysaccharide (LPS) by coupling acid hydrolysis wit
125    Detection of microbial components such as lipopolysaccharide (LPS) by Toll-like receptor 4 (TLR4)
126 noncial inflammasome activation by cytosolic lipopolysaccharide (LPS) causes pyroptotic cell death fa
127 s, whereas the fatty acyl chains attached to lipopolysaccharide (LPS) comprise the hydrophobic portio
128             A study indicated that using the lipopolysaccharide (LPS) core as a ligand, S Typhimurium
129 t's mammary gland immune response to E. coli lipopolysaccharide (LPS) could be conditioned by heat st
130 terestingly, while intracellular delivery of lipopolysaccharide (LPS) derived from Escherichia coli w
131                           Mice injected with lipopolysaccharide (LPS) display a depressive-like pheno
132 h the extracellular surface of OmpF and that lipopolysaccharide (LPS) enhances this binding.
133 gth of acyl groups on the lipid A portion of lipopolysaccharide (LPS) for the enteric pathogens Yersi
134 ram-negative bacteria, O-antigen segments of lipopolysaccharide (LPS) form a chemomechanical barrier,
135                                              Lipopolysaccharide (LPS) from the Gram-negative bacteria
136 though hepatocellular changes in response to lipopolysaccharide (LPS) have been well characterized, l
137                         Here, we showed that lipopolysaccharide (LPS) in combination with IFN-gamma i
138  was used to determine circulating levels of lipopolysaccharide (LPS) in control and CRC populations.
139                      Here, we used bacterial lipopolysaccharide (LPS) in female C57BL/6J mice and acu
140 the inner leaflet and the complex glycolipid lipopolysaccharide (LPS) in the outer leaflet.
141 glet model we assessed the effect of E. coli lipopolysaccharide (LPS) infusion started 4 h prior to a
142  rotundus to test how an immune challenge by lipopolysaccharide (LPS) injections affects two differen
143 ng triggers rapid Ca2+ influx, which induces lipopolysaccharide (LPS) internalisation, followed by ac
144                 In addition, increased blood lipopolysaccharide (LPS) levels during SIV infection wer
145 ins, mucosal inulin permeability, and plasma lipopolysaccharide (LPS) levels.
146 : the chronic unpredictable stress (CUS) and lipopolysaccharide (LPS) models.
147          The membrane surface is composed of lipopolysaccharide (LPS) molecules with negatively charg
148 imurium and Enteritidis, were assessed using lipopolysaccharide (LPS) O antigen-specific antibodies.
149                                              Lipopolysaccharide (LPS) O-antigen (O-Ag) is known to li
150                                          The lipopolysaccharide (LPS) of B. pertussis is an attractiv
151 n mice exposed to a pro-allergic low dose of lipopolysaccharide (LPS) or a protective high dose of LP
152          Equivalent hypoglycemia, induced by lipopolysaccharide (LPS) or insulin, was sufficient to t
153 (HF(-)) and given intrauterine injections of lipopolysaccharide (LPS) or phosphate-buffered saline (P
154 ord blood samples, as well as in response to lipopolysaccharide (LPS) or phytohemagglutinin (PHA) sti
155 ice or high-fat diet induced obese mice with lipopolysaccharide (LPS) or vehicle via endotracheal inj
156 r damage and liver failure models induced by lipopolysaccharide (LPS) plus D-galactosamine (D-Galn),
157 creased Trem2 expression under conditions of lipopolysaccharide (LPS) pro-inflammatory or IL-4 anti-i
158 Further mechanistic studies suggest that the lipopolysaccharide (LPS) purified from R. australis toge
159 ri-induced cell death requires the cytosolic lipopolysaccharide (LPS) receptor caspase-11 and antagon
160                                              Lipopolysaccharide (LPS) resides in the outer membrane o
161                        In vivo, responses to lipopolysaccharide (LPS) result in IL-1beta secretion.
162 e brains of the mice treated with peripheral lipopolysaccharide (LPS) revealed that the cerebral vasc
163                     We focus specifically on lipopolysaccharide (LPS) signaling to platelets.
164  vascular target of inflammation, induced by lipopolysaccharide (LPS) stimulation.
165 nsynonymous polymorphisms in three essential lipopolysaccharide (LPS) synthesis regulators, lapB (als
166  blood neutrophils and HBECs stimulated with lipopolysaccharide (LPS) than in cells from mild asthma.
167                                Rats received lipopolysaccharide (LPS) to induce endotoxemic shock or
168 , whole blood at 30 days was challenged with lipopolysaccharide (LPS) to measure cytokine secretion;
169 rn C57BL/6 mice treated with intraperitoneal lipopolysaccharide (LPS) to mimic systemic sepsis.
170  in the response of macrophages to bacterial lipopolysaccharide (LPS) were due to intercellular desyn
171 l substituent of heptose I of the inner core lipopolysaccharide (LPS) were unable to propagate phage
172 gent that causes plague, the protein Ail and lipopolysaccharide (LPS)(6) enhance lethality by promoti
173                                              Lipopolysaccharide (LPS), a component of the outer membr
174                                              Lipopolysaccharide (LPS), a toxic byproduct of bacterial
175 neurons were intraperitoneally injected with lipopolysaccharide (LPS), a widely used approach to mode
176                                              Lipopolysaccharide (LPS), an inflammatory stimulus deriv
177 eam of phagocytosis, interferon (IFN)-gamma, lipopolysaccharide (LPS), and adenosine receptors.
178 HlyE), cytolethal distending toxin, S. Typhi lipopolysaccharide (LPS), and S. Typhi membrane preparat
179 he outer membrane of gram-negative bacteria, lipopolysaccharide (LPS), binds NLRP6 directly and induc
180                            In the absence of lipopolysaccharide (LPS), CCR5 adopts a topology consist
181 ures and macrophage under the stimulation of lipopolysaccharide (LPS), KCl and oxygen/glucose depriva
182 , such as K-antigen polysaccharide (KPS) and lipopolysaccharide (LPS), might be important for symbios
183                               In response to lipopolysaccharide (LPS), multiple host defense proteins
184                    We examined the effect of lipopolysaccharide (LPS), on HCO(3) absorption in isolat
185 yl)-1-butanone (NNK), the inflammatory agent lipopolysaccharide (LPS), or both.
186  regulates bicarbonate secretion, detoxifies lipopolysaccharide (LPS), regulates gut microbes, and de
187  underlying the activation of coagulation by lipopolysaccharide (LPS), the major cell-wall component
188 of immune response proteins in comparison to lipopolysaccharide (LPS), underlying the differences bet
189 ions of miR-27a/b were also confirmed in the lipopolysaccharide (LPS)- or activated CD4(+) T cell-tre
190                                          The lipopolysaccharide (LPS)- toll-like receptor-4 (TLR4) pa
191                   Specifically, we show that lipopolysaccharide (LPS)-challenged mice harboring IL-10
192         PI4KIIalpha is recruited to maturing lipopolysaccharide (LPS)-containing phagosomes in an ada
193 s also evaluated in vivo in a mouse model of lipopolysaccharide (LPS)-induced acute lung injury (ALI)
194 vestigated the effects of SIRT7 depletion on lipopolysaccharide (LPS)-induced inflammatory responses
195 C-L also exerted a protective effect against lipopolysaccharide (LPS)-induced inflammatory responses
196  to develop and validate a revised model for lipopolysaccharide (LPS)-induced macrophage activation t
197 the thermoregulatory changes observed during lipopolysaccharide (LPS)-induced systemic inflammation (
198 denosine triphosphate (ATP) to mice enhanced lipopolysaccharide (LPS)-induced TF procoagulant activit
199                                              Lipopolysaccharide (LPS)-mediated intestinal damage, dri
200 r NLRP3- and caspase-1-dependent IL-1beta in lipopolysaccharide (LPS)-primed mouse bone marrow-derive
201 miR-145a mimic, followed by stimulation with lipopolysaccharide (LPS).
202 lammation in mice with a single injection of lipopolysaccharide (LPS).
203  mice were also intranasally challenged with lipopolysaccharide (LPS).
204  septic shock in response to lethal doses of lipopolysaccharide (LPS).
205 use prefrontal cortex specimens treated with lipopolysaccharide (LPS).
206 Cs were incubated with palmitate (PA) and/or lipopolysaccharide (LPS).
207 h potent exogenous TLR2/4 agonist, bacterial lipopolysaccharide (LPS).
208  synthesis in THP-1 macrophages treated with lipopolysaccharide (LPS).
209  TolC and 2) the structural barrier molecule lipopolysaccharide (LPS).
210 with IgG responses to bacterial extracts and lipopolysaccharide (LPS).
211 s in metabolites of bMECs when stimulated by lipopolysaccharide (LPS).
212 cutely inflamed by injection of high dose of lipopolysaccharide (LPS).
213 y response elicited by the administration of lipopolysaccharide (LPS).
214 nts were evaluated by stimulating cells with lipopolysaccharide (LPS).
215 ssed by measuring plasma levels of bacterial lipopolysaccharide (LPS).
216  and animals were fed an HFD or treated with lipopolysaccharide (LPS).
217 immune stimulation by Salmonella typhimurium lipopolysaccharide (LPS).
218 es over time in primary cells in response to lipopolysaccharide (LPS).
219 microglia were stimulated with the endotoxin lipopolysaccharide (LPS).
220 in microglia can be "primed" using bacterial lipopolysaccharide (LPS)/endotoxin, it is unknown whethe
221 induced by stimulation with the TLR4 agonist lipopolysaccharide (LPS); thus, this alternative pre-mRN
222 uses exploit bacterial components, including lipopolysaccharides (LPS) and peptidoglycan (PG), to fac
223                                              Lipopolysaccharides (LPS) are essential envelope compone
224                                              Lipopolysaccharides (LPS) is increased in nonalcoholic f
225 lobacter crescentus S-layer assembles on the lipopolysaccharides (LPS) of the cell surface.
226 cteria exhibits unique lipid asymmetry, with lipopolysaccharides (LPS) residing in the outer leaflet
227 rophils cultured in vitro with the prolonged lipopolysaccharides (LPS) stimulation can effectively de
228 d RAW 264.7 cells were exposed to saliva and lipopolysaccharides (LPS) with and without PRF lysates o
229     The presence of endotoxin, also known as lipopolysaccharides (LPS), as a side product appears to
230 imultaneously adsorbs septic molecules, e.g. lipopolysaccharides (LPS), cytokines and damage- or path
231 cular machinery responsible for transporting lipopolysaccharides (LPS), lipoproteins, and beta-barrel
232                              Using traceable lipopolysaccharides (LPS), we reveal that drainage of th
233 nner leaflet phospholipids and outer leaflet lipopolysaccharides (LPS).
234 behavior following an immune challenge (i.p. lipopolysaccharide [LPS] injection) in mice.
235             Adoptive transfer of mature DCs (lipopolysaccharide [LPS]-induced DCs, DClps) with or wit
236 ss hormonal response to an immune challenge (lipopolysaccharides; LPS).
237                                              Lipopolysaccharides (LPSs) of Gram-negative bacteria com
238  uptake depends on the length of constituent lipopolysaccharide macromolecules.
239 e asymmetry and the complex carbohydrates in lipopolysaccharides make it a daunting task to study the
240 the interacting interfaces and indicate that lipopolysaccharide mediates the contacts between BtuB mo
241 c cell defects including increased levels of lipopolysaccharide, membrane vesiculation, dynamic shrin
242 are attributed to T4SS-dependent delivery of lipopolysaccharide metabolites and peptidoglycan into ho
243 reduced uptake in the brain and periphery of lipopolysaccharide mice compared with the acid-mediated
244       The more conserved lipid A part of the lipopolysaccharide molecule is a major element in the pe
245  how this transporter ensures unidirectional lipopolysaccharide movement across the bridge to the out
246    Exogenous pathogen-derived molecules (eg, lipopolysaccharide, nucleic acids) also translocate from
247 Biochemical assays confirmed the presence of lipopolysaccharides, nucleic acids, and protein in OMVs;
248 rhizose, the monosaccharide component of the lipopolysaccharide O-antigen of the nitrogen-fixing bact
249 e preparation of the repeating unit from the lipopolysaccharide O-antigen of Yersinia enterocolitica
250 ore oligosaccharide structure present in the lipopolysaccharide of Ralstonia solanacearum.
251 peptidoglycans of Gram-positive bacteria and lipopolysaccharides of Gram-negative bacteria.
252                     After restimulation with lipopolysaccharide on day 6, (nor)adrenaline-exposed cel
253 ects of chronic neuroinflammation induced by lipopolysaccharides on hippocampal glutamatergic and GAB
254  reacts to neophobia and sickness induced by lipopolysaccharide or cisplatin.
255  some cases could be explained by binding to lipopolysaccharides or capsular polysaccharides, but in
256                   Bacterial products such as lipopolysaccharides (or endotoxin) cause systemic inflam
257 n NAFLD when challenged with a Western diet, lipopolysaccharide, or CoCl2.
258 en stimulated with amyloid beta42 oligomers, lipopolysaccharides, or dexamethasone.
259 g/mL pre-lipopolysaccharide to 54 pg/mL post-lipopolysaccharide, P<0.001.
260 haride (Ec-LPS) and Porphyromonas gingivalis lipopolysaccharide (Pg-LPS) stimulation, using enzyme-li
261 trapure or standard Porphyromonas gingivalis lipopolysaccharide (PgLPS), Pam3CSK4, or interferon-gamm
262 ged with the classical inflammasome model of lipopolysaccharide plus adenosine triphosphate, PRL inhi
263    As predicted by current models, bacterial lipopolysaccharide polarizes the immune response such th
264                     While cells activated by lipopolysaccharide rely exclusively on glycolysis, macro
265 e to a synthetic triacylated lipopeptide and lipopolysaccharide, respectively, as well as an endogeno
266           These structures resolve the bound lipopolysaccharide, reveal transporter-lipopolysaccharid
267                          Upregulation of the lipopolysaccharide sensor caspase-11 in the intestines o
268                                          How lipopolysaccharide sequestered in the membranes of cytos
269 , the administration of DMF protects against lipopolysaccharide shock and alleviates familial Mediter
270 ive microbiome driving CA lesion genesis via lipopolysaccharide signaling, in humans as in mice.
271 ying TNF-alpha in the cell culture medium of lipopolysaccharide stimulated and non-stimulated astrocy
272 PBMCs both from septic patients (n = 10) and lipopolysaccharide stimulated PBMCs from healthy volunte
273              These findings were mirrored in lipopolysaccharide stimulated PBMCs taken from healthy v
274 vity of protein hydrolysates was assessed in lipopolysaccharide-stimulated HT-29 cells using ELISA as
275  exhibited capacity to decrease NO levels in lipopolysaccharide-stimulated murine macrophage-like cel
276 hat iRhom2 also is present on the surface of lipopolysaccharide-stimulated primary bone marrow-derive
277                          13-LAHLA suppresses lipopolysaccharide-stimulated secretion of cytokines and
278 in resistance - TNF, IL-1beta, and CCL2 - by lipopolysaccharide-stimulated THP-1 cells.
279 s required for prostacyclin production after lipopolysaccharide stimulation and optimal induction of
280 d decreased TNFalpha secretion after ex vivo lipopolysaccharide stimulation compared with their Ucp2(
281                                 Furthermore, lipopolysaccharide stimulation of murine RAW 264.7 cells
282 n (RBP) human antigen R (HuR) in response to lipopolysaccharide stimulation, but the role of other re
283 te-differentiated macrophages in response to lipopolysaccharide stimulation.
284                                       In the lipopolysaccharide study, median NT-proBNP levels rose f
285 ement is independent of a role in regulating lipopolysaccharide synthesis, as has been suggested for
286 ts are activated by the bacterial endotoxin, lipopolysaccharide, that is released from the gastrointe
287 dian NT-proBNP levels rose from 21 pg/mL pre-lipopolysaccharide to 54 pg/mL post-lipopolysaccharide,
288 via the non-canonical inflammasome, and that lipopolysaccharide transfection into the host cytoplasm
289 4)Cu]Cu-c[E(4)W(5)C] uptake in the brains of lipopolysaccharide-treated animals.
290 , hippocampus, striatum, and hypothalamus of lipopolysaccharide-treated mice (vs.
291 64)Cu]Cu-c[E(4)W(5)C] uptake was observed in lipopolysaccharide-treated mice (vs.
292                                  Of note, in lipopolysaccharide-treated or Sendai virus-infected U937
293                                              Lipopolysaccharide treatment led to the deposition of NE
294                                              Lipopolysaccharide treatment rapidly enhanced atheroscle
295                                    Bacterial lipopolysaccharide triggers human caspase-4 (murine casp
296 cytic cell line) macrophages stimulated with lipopolysaccharide using Hi-C coupled with sequence capt
297                The hematopoietic response to lipopolysaccharide was also mitigated after a previous M
298                    In contrast, gossypol and lipopolysaccharides were toxic to macrophages but not ad
299 outer membrane composed of phospholipids and lipopolysaccharide, which acts as a barrier and contribu
300  pro-inflammatory stimulus such as bacterial lipopolysaccharide, which may implicate a compromised ca

 
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