a(CHEBI:lipopolysaccharide)
We showed that simulation of macrophages with LPS resulted in significant reduction in ferroportin mRNA and protein expression and enhanced intracellular iron deposition throughout all time points tested (Fig. 5A–D). PubMed:29212341
This dramatically contrasts the iron phenotype that develops in response to LPS, hallmarked by high intracellular iron levels and low ferroportin expression (10, 20, 48). PubMed:29212341
We showed that simulation of macrophages with LPS resulted in significant reduction in ferroportin mRNA and protein expression and enhanced intracellular iron deposition throughout all time points tested (Fig. 5A–D). PubMed:29212341
This dramatically contrasts the iron phenotype that develops in response to LPS, hallmarked by high intracellular iron levels and low ferroportin expression (10, 20, 48). PubMed:29212341
We showed that simulation of macrophages with LPS resulted in significant reduction in ferroportin mRNA and protein expression and enhanced intracellular iron deposition throughout all time points tested (Fig. 5A–D). PubMed:29212341
An increased STAT3 (Mann–Whitney U=0, Z=-2.309, P=0.021) and p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-2.309, p=0.021) was observed in LPS treated microglia (Fig. 3) PubMed:23178521
We observed that anatabine significantly suppressed the stimulation of p65 NFkB and STAT3 phosphorylation by LPS in microglia (Fig. 3) PubMed:23178521
Following a 24 h incubation with LPS, a significant stimulation of STAT3 (Mann– Whitney U=0, Z=-2.882, P=0.004) and p65 NFkB phosphorylation was observed (Mann–Whitney U=1, Z=-2.722, P=0.006) PubMed:23178521
An increased STAT3 (Mann–Whitney U=0, Z=-2.309, P=0.021) and p65 NFkB phosphorylation (Mann–Whitney U=0, Z=-2.309, p=0.021) was observed in LPS treated microglia (Fig. 3) PubMed:23178521
We observed that anatabine significantly suppressed the stimulation of p65 NFkB and STAT3 phosphorylation by LPS in microglia (Fig. 3) PubMed:23178521
Similarly, LPS induced p65 NFkB phosphorylation in microglia was significantly inhibited with 10 mg/ml of anatabine (Mann–Whitney U=0, Z=-2.309, P=0.021), with 100 mg/ml of anatabine (Mann– Whitney U=0, Z=-2.309, P=0.021), with 300 mg/ml of anatabine (Mann–Whitney U=0, Z=-2.309, P=0.021) PubMed:23178521
Following a 24 h incubation with LPS, a significant stimulation of STAT3 (Mann– Whitney U=0, Z=-2.882, P=0.004) and p65 NFkB phosphorylation was observed (Mann–Whitney U=1, Z=-2.722, P=0.006) PubMed:23178521
Anatabine at 200 mg/ ml significantly lowered LPS induced IL-1b levels in whole blood (Mann–Whitney U=0.0, Z=-2.3, P=0.02) PubMed:23178521
Our results showed that intraperitoneal injection of LPS (1 mg/kg) caused a significant elevation of plasma IL-1b (Mann–Whitney U=3, Z=-2.988, P=0.003), IL-6 (Mann–Whitney U=0, Z=-3.366, P=0.001) and TNFa (Mann– Whitney U=0, Z=-3.508, P<0.001) 4 h after the LPS challenge whereas in mice co-treated with an intraperitoneal injection of anatabine (2 mg/kg) and LPS, a significant reduction in plasma IL-1b (Mann–Whitney U=7, Z=-2.645, P=0.008) and TNFa (Mann–Whitney U=4, Z=-2.941, P=0.003) levels was observed (Fig. 6) PubMed:23178521
An elevation of IL-6 (Mann–Whitney U=0, Z=-3.487, P<0.001), IL1b (Mann– Whitney U=0, Z=-3.24, P=0.001) and TNFa (Mann–Whitney U=0, Z=-3.361, P=0.001) was observed in the spleen of LPS challenged mice (Fig. 7) PubMed:23178521
Similarly, IL-1b (Mann–Whitney U=0, Z=-3.098, P=0.002), IL-6 (Mann–Whitney U=0, Z=-3.363, P<0.001) and TNF-a levels (Mann–Whitney U=0, Z=-3.361, P=0.001) were elevated in the kidney following the LPS challenge (data not shown) PubMed:23178521
Our results showed that intraperitoneal injection of LPS (1 mg/kg) caused a significant elevation of plasma IL-1b (Mann–Whitney U=3, Z=-2.988, P=0.003), IL-6 (Mann–Whitney U=0, Z=-3.366, P=0.001) and TNFa (Mann– Whitney U=0, Z=-3.508, P<0.001) 4 h after the LPS challenge whereas in mice co-treated with an intraperitoneal injection of anatabine (2 mg/kg) and LPS, a significant reduction in plasma IL-1b (Mann–Whitney U=7, Z=-2.645, P=0.008) and TNFa (Mann–Whitney U=4, Z=-2.941, P=0.003) levels was observed (Fig. 6) PubMed:23178521
An elevation of IL-6 (Mann–Whitney U=0, Z=-3.487, P<0.001), IL1b (Mann– Whitney U=0, Z=-3.24, P=0.001) and TNFa (Mann–Whitney U=0, Z=-3.361, P=0.001) was observed in the spleen of LPS challenged mice (Fig. 7) PubMed:23178521
Similarly, IL-1b (Mann–Whitney U=0, Z=-3.098, P=0.002), IL-6 (Mann–Whitney U=0, Z=-3.363, P<0.001) and TNF-a levels (Mann–Whitney U=0, Z=-3.361, P=0.001) were elevated in the kidney following the LPS challenge (data not shown) PubMed:23178521
Our results showed that intraperitoneal injection of LPS (1 mg/kg) caused a significant elevation of plasma IL-1b (Mann–Whitney U=3, Z=-2.988, P=0.003), IL-6 (Mann–Whitney U=0, Z=-3.366, P=0.001) and TNFa (Mann– Whitney U=0, Z=-3.508, P<0.001) 4 h after the LPS challenge whereas in mice co-treated with an intraperitoneal injection of anatabine (2 mg/kg) and LPS, a significant reduction in plasma IL-1b (Mann–Whitney U=7, Z=-2.645, P=0.008) and TNFa (Mann–Whitney U=4, Z=-2.941, P=0.003) levels was observed (Fig. 6) PubMed:23178521
An elevation of IL-6 (Mann–Whitney U=0, Z=-3.487, P<0.001), IL1b (Mann– Whitney U=0, Z=-3.24, P=0.001) and TNFa (Mann–Whitney U=0, Z=-3.361, P=0.001) was observed in the spleen of LPS challenged mice (Fig. 7) PubMed:23178521
Similarly, IL-1b (Mann–Whitney U=0, Z=-3.098, P=0.002), IL-6 (Mann–Whitney U=0, Z=-3.363, P<0.001) and TNF-a levels (Mann–Whitney U=0, Z=-3.361, P=0.001) were elevated in the kidney following the LPS challenge (data not shown) PubMed:23178521
Western-blot experiments revealed that LPS significantly stimulated of STAT3 phosphorylation in the spleen (Mann–Whitney U=0, Z=-2.309, P=0.021) (Fig. 8) and kidney (Mann–Whitney U=0, Z=-2.882, P=0.004) (data not shown) whereas anatabine significantly inhibited STAT3 phosphorylation in the spleen (Mann–Whitney U=1, Z=-2.021, P=0.043) and kidney (Mann– Whitney U=5, Z=-2.082, P=0.037) (data not shown) PubMed:23178521
Anatabine suppressed in a dose- dependent manner the increase of iNOS and COX2 in- duced by interferon-g (Fig.4),confirming in vitro its antiinflammatory properties. The effect seen with inter- feron-g was also seen when macrophages were stimulated with lipopolysaccharide (Supplemental Fig. 1). PubMed:22807490
Transfusion of RBCs after prolonged refrigerator storage is associated with haemolysis (Donadee et al, 2011; Hod et al, 2011) and enhances cytokine secretion in response to lipopolysaccharide (LPS) administration (Hod et al, 2010). PubMed:25307023
We showed that simulation of macrophages with LPS resulted in significant reduction in ferroportin mRNA and protein expression and enhanced intracellular iron deposition throughout all time points tested (Fig. 5A–D). PubMed:29212341
We showed that simulation of macrophages with LPS resulted in significant reduction in ferroportin mRNA and protein expression and enhanced intracellular iron deposition throughout all time points tested (Fig. 5A–D). PubMed:29212341
This dramatically contrasts the iron phenotype that develops in response to LPS, hallmarked by high intracellular iron levels and low ferroportin expression (10, 20, 48). PubMed:29212341
We showed that simulation of macrophages with LPS resulted in significant reduction in ferroportin mRNA and protein expression and enhanced intracellular iron deposition throughout all time points tested (Fig. 5A–D). PubMed:29212341
This dramatically contrasts the iron phenotype that develops in response to LPS, hallmarked by high intracellular iron levels and low ferroportin expression (10, 20, 48). PubMed:29212341
In animal experiments, the administration of lipopolysaccharide (LPS) to induce systemic inflammation leads to a significant increase in plasma concentration of cell-free hemoglobin as well [5–8]. PubMed:29956069
Due to these properties, LPS can easily be incorporated into the membrane of (red blood) cells, alter their membrane properties, and thus promote cell death [123, 124]. PubMed:29956069
We found, moreover, a decreased osmotic resistance and membrane stiffness of washed red blood cells treated with LPS [80, 81]. PubMed:29956069
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.