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10 ng/ml lipopolysaccharide (lps)  (ImmunoTools)
90
ImmunoTools 10 ng/ml lipopolysaccharide (lps)
10 Ng/Ml Lipopolysaccharide (Lps), supplied by ImmunoTools, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/lps+plus+10+ng/10+ng+ml+lipopolysaccharide++lps+/pm39542199-152-14-22
Average 90 stars, based on 1 article reviews
10 ng/ml lipopolysaccharide (lps) - by Bioz Stars, 2026-10
90/100 stars
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ultra pure e. coli lps 0111:b4 0111:b4  (Vivogen Biotechnology Inc)
90
Vivogen Biotechnology Inc ultra pure e. coli lps 0111:b4 0111:b4
Ultra Pure E. Coli Lps 0111:B4 0111:B4, supplied by Vivogen Biotechnology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/lps+plus+10+ng/10+ng+ml+of+lipopolysaccharide++lps++0111++b4++escherichia+coli+/pm36225929-189-25-31
Average 90 stars, based on 1 article reviews
ultra pure e. coli lps 0111:b4 0111:b4 - by Bioz Stars, 2026-10
90/100 stars
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lps 10 ng/ml  (EMC microcollections GmbH)
90
EMC microcollections GmbH lps 10 ng/ml
High-fat-shake-induced trained immunity is regulated via TLR4 but is not mediated via low-dose LPS, triglyceride-rich lipoproteins, or the saturated fatty acids that are particularly increased after the high-fat shake (A) Adherent human monocytes were pre-incubated for 1 h with plain <t>RPMI</t> or Bartonella LPS (B. LPS). After pre-incubation, the cells were exposed for 24 h to high-fat serum obtained at t = 0 h (HFS0) or at t = 6 h (HFS6), with (PB) or without neutralization of LPS. On day 6, cells were restimulated for 24 h and cytokine production was measured ( n = 8). Data are presented as fold of change to HFS0 for each separate inhibitor. (B) HFS0 and HFS6 were depleted from apoB-containing lipoproteins before use in the training experiments ( n = 6). (C) The fatty acid composition of the pooled serum obtained at t = 6 h after consumption of the high-fat and the reference shake. Lauric acid (FA(12:0)) a , myristic acid (FA(14:0)) a , and stearic acid (FA(18:0)) a were particularly higher in the high-fat serum. Palmitoleic acid (FA(16:1)) a , oleic acid (FA(18:1)) a , and linoleic acid (FA(18:2)) a were lower. (D) Monocytes <t>were</t> <t>stimulated</t> for 24 h with albumin-conjugated C12:0, C14:0, and C18:0 or with the albumin vehicle (Alb) alone. After resting and differentiation, cytokine production upon restimulation was measured ( n = 8). (E) The same inhibition experiments as described under (A) were performed for C12:0 and C14:0. Data are presented as fold of change to the vehicle control for each separate inhibitor (B. LPS n = 10, PB n = 9). Median ± IQR. ∗ indicates two-sided p < 0.05, ∗∗ p < 0.01, Wilcoxon signed-rank test. See also <xref ref-type=Figures S3 and . " width="250" height="auto" />
Lps 10 Ng/Ml, supplied by EMC microcollections GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/lps+plus+10+ng/lps+10+ng+ml/pmc11530819-352-17-29
Average 90 stars, based on 1 article reviews
lps 10 ng/ml - by Bioz Stars, 2026-10
90/100 stars
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High-fat-shake-induced trained immunity is regulated via TLR4 but is not mediated via low-dose LPS, triglyceride-rich lipoproteins, or the saturated fatty acids that are particularly increased after the high-fat shake (A) Adherent human monocytes were pre-incubated for 1 h with plain RPMI or Bartonella LPS (B. LPS). After pre-incubation, the cells were exposed for 24 h to high-fat serum obtained at t = 0 h (HFS0) or at t = 6 h (HFS6), with (PB) or without neutralization of LPS. On day 6, cells were restimulated for 24 h and cytokine production was measured ( n = 8). Data are presented as fold of change to HFS0 for each separate inhibitor. (B) HFS0 and HFS6 were depleted from apoB-containing lipoproteins before use in the training experiments ( n = 6). (C) The fatty acid composition of the pooled serum obtained at t = 6 h after consumption of the high-fat and the reference shake. Lauric acid (FA(12:0)) a , myristic acid (FA(14:0)) a , and stearic acid (FA(18:0)) a were particularly higher in the high-fat serum. Palmitoleic acid (FA(16:1)) a , oleic acid (FA(18:1)) a , and linoleic acid (FA(18:2)) a were lower. (D) Monocytes were stimulated for 24 h with albumin-conjugated C12:0, C14:0, and C18:0 or with the albumin vehicle (Alb) alone. After resting and differentiation, cytokine production upon restimulation was measured ( n = 8). (E) The same inhibition experiments as described under (A) were performed for C12:0 and C14:0. Data are presented as fold of change to the vehicle control for each separate inhibitor (B. LPS n = 10, PB n = 9). Median ± IQR. ∗ indicates two-sided p < 0.05, ∗∗ p < 0.01, Wilcoxon signed-rank test. See also <xref ref-type=Figures S3 and . " width="100%" height="100%">

Journal: iScience

Article Title: Single high-fat challenge and trained innate immunity: A randomized controlled cross-over trial

doi: 10.1016/j.isci.2024.111103

Figure Lengend Snippet: High-fat-shake-induced trained immunity is regulated via TLR4 but is not mediated via low-dose LPS, triglyceride-rich lipoproteins, or the saturated fatty acids that are particularly increased after the high-fat shake (A) Adherent human monocytes were pre-incubated for 1 h with plain RPMI or Bartonella LPS (B. LPS). After pre-incubation, the cells were exposed for 24 h to high-fat serum obtained at t = 0 h (HFS0) or at t = 6 h (HFS6), with (PB) or without neutralization of LPS. On day 6, cells were restimulated for 24 h and cytokine production was measured ( n = 8). Data are presented as fold of change to HFS0 for each separate inhibitor. (B) HFS0 and HFS6 were depleted from apoB-containing lipoproteins before use in the training experiments ( n = 6). (C) The fatty acid composition of the pooled serum obtained at t = 6 h after consumption of the high-fat and the reference shake. Lauric acid (FA(12:0)) a , myristic acid (FA(14:0)) a , and stearic acid (FA(18:0)) a were particularly higher in the high-fat serum. Palmitoleic acid (FA(16:1)) a , oleic acid (FA(18:1)) a , and linoleic acid (FA(18:2)) a were lower. (D) Monocytes were stimulated for 24 h with albumin-conjugated C12:0, C14:0, and C18:0 or with the albumin vehicle (Alb) alone. After resting and differentiation, cytokine production upon restimulation was measured ( n = 8). (E) The same inhibition experiments as described under (A) were performed for C12:0 and C14:0. Data are presented as fold of change to the vehicle control for each separate inhibitor (B. LPS n = 10, PB n = 9). Median ± IQR. ∗ indicates two-sided p < 0.05, ∗∗ p < 0.01, Wilcoxon signed-rank test. See also Figures S3 and .

Article Snippet: After the resting period, cells were stimulated for a second time during another 24 h with either RPMI, LPS 10 ng/mL (TLR4 agonist) or Pam3CysK4 (P3C) 10 μg/mL (L2000, EMC Microcollections; TLR2 agonist).

Techniques: Incubation, Neutralization, Inhibition, Control

Journal: iScience

Article Title: Single high-fat challenge and trained innate immunity: A randomized controlled cross-over trial

doi: 10.1016/j.isci.2024.111103

Figure Lengend Snippet:

Article Snippet: After the resting period, cells were stimulated for a second time during another 24 h with either RPMI, LPS 10 ng/mL (TLR4 agonist) or Pam3CysK4 (P3C) 10 μg/mL (L2000, EMC Microcollections; TLR2 agonist).

Techniques: Recombinant, Saline, Enzyme-linked Immunosorbent Assay, Software, Flow Cytometry