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244 results for “lipopolysaccharide”
Figure 11 in All aspects of the toxic effects of lipopolysaccharide on rat liver and the protective effect of vitamin E and sodium selenite
Figure 11. DNA damage in rat liver exposed to LPS + VE and/or SS. (a) Control group, (b) VE, (c) SS, (d, e) LPS, (f) LPS + VE, (g) LPS + SS, and (h, i) LPS + VE + SS groups.
Figure 10 in All aspects of the toxic effects of lipopolysaccharide on rat liver and the protective effect of vitamin E and sodium selenite
Figure 10. Histological features of the apoptotic areas in the liver of the rats. A, B, C → Control; D, E, F → SS; G, H, I →VE; J, K, L → SS + VE; M, N, O → LPS; P, Q, R → LPS + SS; S, T, U, → LPS + VE; and V, W, X → LPS + SS + VE.
Figure 6 in All aspects of the toxic effects of lipopolysaccharide on rat liver and the protective effect of vitamin E and sodium selenite
Figure 6. Liver sections of the LPS + SS-treated rats. Showing (A) ⇑: dilation of the sinusoids, *: necrosis, and ►: vacuolar degeneration; and (B) ↑↑: vascular congestion and ⇒: hemorrhage at 200×.
Figure 4 in All aspects of the toxic effects of lipopolysaccharide on rat liver and the protective effect of vitamin E and sodium selenite
Figure 4. Liver sections of the LPS-treated rats. (A) Showing Δ: leukocyte infiltration, *: necrosis, Δ: dilation of the sinusoids at 200×; (B) ►: vacuolar degeneration, →: binucleated hepatocytes at 400×; (C) ⇒: hemorrhage, Δ: leukocyte infiltration, *: necrosis, ↑↑: vascular congestion; and (D) ⇑: dilation of the sinusoids and *: necrosis at 200×.
Figure 3 in All aspects of the toxic effects of lipopolysaccharide on rat liver and the protective effect of vitamin E and sodium selenite
Figure 3. Liver section of the control rats, CV: central vein at 200×. Histological structures (A, B) of the control, VE, SS, and VE + SStreated rats were similar to the control group.
Figure 2 in All aspects of the toxic effects of lipopolysaccharide on rat liver and the protective effect of vitamin E and sodium selenite
Figure 2. TEAC values (μmol of Trolox equiv/gram tissue) in the liver of rats treated with LPS (10 mg/kg bw), VE (200 mg/kg bw), and SS (0.35 mg/kg bw). Significance was accepted as P <0.05.
Figure 1 in All aspects of the toxic effects of lipopolysaccharide on rat liver and the protective effect of vitamin E and sodium selenite
Figure 1. FRAP values (μmol of FeII equiv/gram tissue) in the liver of rats treated with LPS (10 mg/kg bw), VE (200 mg/kg bw), and SS (0.35 mg/kg bw). Significance was accepted as P <0.05.
Differentially-expressed genes in blood in response to lipopolysaccharide in three rodent species
<p>Infection tolerance in rodents was examined by injecting single-dose lipopolysaccharide (LPS) to induce inflammation in <span><em>Peromyscus</em> <em>leucopus</em></span><span> (LL stock), the white-footed deermouse also reservoir for Lyme disease and </span><span><em>Mus</em> <em>musculus</em></span><span> (outbred CD-1 breed), the house mouse, and </span><span><em>Rattus</em> <em>norvegicus</em></span><span>, the brown rat (Fischer strain). Reaction to LPS was analyzed in the blood of challenged rodents and compared to control animals. As natural reservoirs of zoonoses deermice show significant anti-inflammatory response as described in "An Infection-Tolerant Mammalian Reservoir for Several Zoonotic Agents Broadly Counters the Inflammatory Effects of Endotoxin" (</span><a href="https://doi.org/10.1128/mBio.00588-21)" rel="noopener"><span>https://doi.org/10.1128/mBio.00588-21)</span></a><span>. The project and the description of the samples are described under the following NCBI BioProjects: PRJNA975149 (</span><a href="https://www.ncbi.nlm.nih.gov/bioproject/PRJNA975149" rel="noopener"><span>https://www.ncbi.nlm.nih.gov/bioproject/PRJNA975149)</span></a><span> for mouse and deermouse and PRJNA973677 (</span><a href="https://www.ncbi.nlm.nih.gov/bioproject/PRJNA973677)" rel="noopener"><span>https://www.ncbi.nlm.nih.gov/bioproject/PRJNA973677)</span></a><span>. This project is a follow-up project focusing on the transcriptomic analysis of the whole blood bulk RNA-seq and further analysis of differentially expressed genes (DEG) between the treatment arm and controls. Complete fold change and false discovery rate for all three rodent species used for the current Dryad set are previously published (<a href="https://doi.org/10.7280/D1470Z">https://doi.org/10.7280/D1470Z</a>). Here we report that deermice tolerance to infection is partly due to lower expression of interferon-gamma in comparison to mice and rats. <br></span></p>
Feasibility Study of Intra-Tumoral Lipopolysaccharide Immunotherapy for Intra-Abdominal
ClinicalTrials.gov study NCT05751837. IPD Sharing: NO. Countries: 1. Publications: 19.
Differentially-expressed genes in blood in response to lipopolysaccharide in three rodent species
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Raw Data for the article: Klebsiella pneumoniae Lipopolysaccharides Serotype O2afg Induce Poor Inflammatory Immune Responses Ex Vivo
<p>Currently, <em>Klebsiella pneumoniae</em> is a pathogen of clinical relevance due to its plastic ability of acquiring resistance genes to multiple antibiotics. During <em>K. pneumoniae</em> infections, lipopolysaccharides (LPS) play an ambiguous role as they both activate immune responses but can also play a role in immune evasion. The LPS O2a and LPS O2afg serotypes are prevalent in most multidrug resistant <em>K. pneumoniae</em> strains. Thus, we sought to understand if those two particular LPS serotypes were involved in a mechanism of immune evasion. We have extracted LPS (serotypes O1, O2a and O2afg) from <em>K. pneumoniae</em> strains and, using human monocytes ex vivo, we assessed the ability of those LPS antigens to induce the production of pro-inflammatory cytokines and chemokines. We observed that, when human monocytes are incubated with LPS serotypes O1, O2a or O2afg strains, O2afg and, to a lesser extent, O2a but not O1 failed to elicit the production of pro-inflammatory cytokines and chemokines, which suggests a role in immune evasion. Our preliminary data also shows that nuclear translocation of NF-κB, a process which regulates an immune response against infections, occurs in monocytes incubated with LPS O1 and, to a smaller extent, with LPS O2a, but not with the LPS serotype O2afg. Our results indicate that multidrug resistant <em>K. pneumoniae</em> expressing LPS O2afg serotypes avoid an initial inflammatory immune response and, consequently, are able to systematically spread inside the host unharmed, which results in the several pathologies associated with this bacterium.</p>
The role of the essential GTPase ObgE in regulating lipopolysaccharide synthesis in Escherichia coli
<p>Source data accompanying scientific publication.</p> <p>Abstract: <span>During growth, cells need to synthesize and expand their envelope, a process that requires careful regulation. Here, we show that the GTPase ObgE of <em>E. coli</em> contributes to the regulation of lipopolysaccharide (LPS) synthesis, an essential component of the Gram-negative outer membrane. Using a dominant-negative mutant (named ‘ObgE*’), we show a direct interaction between ObgE and LpxA, which catalyzes the first step in LPS synthesis. This interaction is enhanced by the mutation in ObgE* which, when bound to GTP, leads to inhibition of LpxA, decreased LPS synthesis, and cell death. Although wild-type ObgE does not exert the same strong effects as ObgE* on LpxA or LPS synthesis, our data indicate that ObgE participates in the regulation of cell envelope synthesis in <em>E. coli</em>. Because ObgE also influences other cellular functions (i.e., ribosome assembly, DNA replication, etc.), it seems increasingly plausible that this GTPase coordinates several processes to finetune cell growth.</span></p>
High prevalence of lipopolysaccharide mutants and R2-Pyocin susceptible variants in Pseudomonas aeruginosa populations sourced from cystic fibrosis lung infections
<p>Chronic, highly antibiotic-resistant infections in cystic fibrosis (CF) lungs contribute to increasing morbidity and mortality. <em>Pseudomonas</em> <em>aeruginosa</em>, a common CF pathogen, exhibits resistance to multiple antibiotics, contributing to antimicrobial resistance (AMR). These bacterial populations display genetic and phenotypic diversity, but it is unclear how this diversity affects susceptibility to bacteriocins. R-pyocins, i.e. bacteriocins produced by <em>P. aeruginosa</em>, are phage-tail-like antimicrobials. R-pyocins have potential as antimicrobials, however, recent research suggests the diversity of <em>P. aeruginosa</em> variants within CF lung infections leads to varying susceptibility to R-pyocins. This variation may be linked to changes in lipopolysaccharide (LPS), acting as the R-pyocin receptor. Currently, it is unknown how frequently R-pyocin-susceptible strains are in chronic CF lung infection, particularly when considering the heterogeneity within these strains. In this study, we tested R2-pyocin susceptibility of 139 <em>P. aeruginosa</em> variants from 17 sputum samples of seven CF patients and analyzed LPS phenotypes. We found that 83% of sputum samples did not have R2-pyocin-resistant variants, while nearly all samples contained susceptible variants. There was no correlation between LPS phenotype and R2-pyocin susceptibility, though we estimate that about 76% of sputum-derived variants lack an O-specific antigen, 40% lack a common antigen, and 24% have altered LPS cores. The absence of a correlation between LPS phenotype and R-pyocin susceptibility suggests LPS packing density may play a significant role in R-pyocin susceptibility among CF variants. Our research supports the potential of R-pyocins as therapeutic agents, as many infectious CF variants are susceptible to R2-pyocins, even within diverse bacterial populations.</p>
Effects of GSK2798745 on Alveolar Barrier Disruption in a Segmental Lipopolysaccharide (LPS) Challenge Model
ClinicalTrials.gov study NCT03511105. IPD Sharing: YES. Countries: 1. Publications: 1.
Differential avoidance of the odour of opposite sex mice receiving acute and repeated Lipopolysaccharide
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Colistin kills bacteria by targeting lipopolysaccharide in the cytoplasmic membrane - primary data for all experiments described in the manuscript
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Dynamic basis of lipopolysaccharide export by LptB2FGC
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High prevalence of lipopolysaccharide mutants and R2-Pyocin susceptible variants in Pseudomonas aeruginosa populations sourced from cystic fibrosis lung infections
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Differentially expressed genes of Peromyscus leucopus fibroblast cultures treated with lipopolysaccharide or buffer alone
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Differentially expressed genes in the blood, spleen, and liver of Peromyscus leucopus and Mus musculus with or without treatment with lipopolysaccharide
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
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DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
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