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Dariusz Szukiewicz - One of the best experts on this subject based on the ideXlab platform.
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Anti-inflammatory Action of Metformin with Respect to CX3CL1/CX3CR1 Signaling in Human Placental Circulation in Normal-Glucose Versus High-Glucose Environments
Inflammation, 2018Co-Authors: Dariusz Szukiewicz, Michal Bachanek, Seweryn Trojanowski, Habib Alkhalayla, Aleksandra Stangret, Grzegorz Szewczyk, Michal Pyzlak, Jaroslaw WejmanAbstract:Upregulation of Chemokine CX3CL1 and its receptor CX3CR1 occurs in the diabetic human placenta. Metformin, an insulin-sensitizing biguanide, is used in the therapy of diabetic pregnancy. By preventing the activation of NF-κB, metformin exhibits anti-inflammatory properties. We examined the influence of hyperglycemia (25 mmol/L glucose; HG group; N = 36) on metformin-mediated effects on CX3CL1 and TNF-α production by placental lobules perfused extracorporeally. Additionally, CX3CR1 expression and contents of CX3CR1, TNF-α receptor 1 (TNFR1), and NF-κB proteins in the placental tissue were evaluated. Placentae perfused under normoglycemia (5 mmol/L glucose; NG group; N = 36) served as the control. Metformin (2.5 and 5.0 mg/L; subgroups B and C) lowered the production of CX3CL1 and TNF-α in a dose-dependent and time-dependent manner. Hyperglycemia did not weaken the strength of these metformin effects. Moreover, CX3CL1 levels after perfusion with 5.0 mg/L metformin were reduced by 33.28 and 33.83% (at 120 and 150 min, respectively) in the HG-C subgroup versus 24.98 and 23.66% in the NG-C subgroup, which indicated an augmentation of the metformin action over time in hyperglycemia. CX3CR1 expression was significantly higher in the HG-B and HG-C subgroups compared to that in the NG-B and NG-C subgroups. Increased CX3CR1 protein content in the placental lysates was observed in subgroups B and C. The two higher metformin concentrations significantly decreased the levels of NF-κBp65 protein content in both groups. However, the decrease was significantly stronger in hyperglycemia. TNFR1 upregulation in the HG group was not affected by metformin. Further studies on metformin therapy during pregnancy are needed, including safety issues.
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High Glucose Level Disturbs the Resveratrol-Evoked Curtailment of CX3CL1/CX3CR1 Signaling in Human Placental Circulation.
Mediators of Inflammation, 2017Co-Authors: Dariusz Szukiewicz, Michal Bachanek, Seweryn Trojanowski, Aleksandra Stangret, Grzegorz Szewczyk, Michal Pyzlak, Wojciech Braksator, Jaroslaw WejmanAbstract:Hyperglycemia-induced hyperactivity of Chemokine CX3CL1 (fractalkine) occurs in the human placenta. Anti-inflammatory/antioxidant activities of resveratrol (3,5,4'-trihydroxy-trans-stilbene) are related to the modulation of Chemokine CX3CL1 and its receptor, CX3CR1, signaling pathways. We examined the influence of high glucose (25 mmol/L glucose; HG group; N = 36) on resveratrol-mediated effects on CX3CL1 and TNF-α production by the placental lobule, CX3CR1 expression and contents of CX3CR1, TNF-α receptor 1 (TNFR1), and NF-κB proteins in placental tissue. The placental lobules perfused under normoglycemic conditions formed the control NG group (N = 36). Resveratrol (50 and 100 μM; subgroups B and C) administered into the perfusion fluid lowered the production of both CX3CL1 and TNF-α. The reductions in CX3CL1 levels were more evident in the NG group. CX3CR1 expression was significantly higher in the NG subgroups B and C compared to the HG subgroups B and C (385.2 and 426.5% versus 199.3 and 282.4%, resp.). An increase in CX3CR1 protein content in placental lysates was observed in the NG subgroups B and C. Also, resveratrol significantly decreased NF-κBp65 protein content only in the NG group, not affecting hyperglycemia-elicited TNFR1 upregulation. In conclusion, euglycemia assures optimal effects of resveratrol pertaining to CX3CL1/CX3CR1 signaling in the placenta. Future studies on resveratrol are needed, especially those including maternal-fetal risk assessments.
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Aspirin Action in Endothelial Cells: Different Patterns of Response Between Chemokine CX3CL1/CX3CR1 and TNF-α/TNFR1 Signaling Pathways
Cardiovascular Drugs and Therapy, 2015Co-Authors: Dariusz Szukiewicz, Aleksandra Stangret, Grzegorz Szewczyk, Tarun Kumar Mittal, Malgorzata Wojciechowska, Anna Bilska, Mateusz Watroba, Jan KochanowskiAbstract:Purpose TNF-α induces fractalkine (CX3CL1) and its receptor CX3CR1 in endothelial cells through NF-қB activation. NF-қB inhibitors may reduce the expression of CX3CL1, and modulation of the CX3CL1/CX3CR1 signaling was proposed as a new target for aspirin. We examined the effects of aspirin on CX3CL1 and TNF-α production, as well as CX3CR1 and TNFR1 expression. Methods HUVECs isolated after term pregnancies ( N = 28) were cultured in vitro. Lipopolysaccharide (1 μg/ml) was used as CX3CL1 inducer. HUVECs were exposed to six different concentrations of aspirin (between 1.0 and 6.0 mM) during 7 days. The levels of CX3CL1 and TNF-α in the culture media were measured using ELISA. After termination of the cultures, mean expressions of CX3CR1 and TNFR1 were examined in the immunostained paraffin sections using quantitative immunohistochemistry. Results Aspirin significantly ( p
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Aspirin Action in Endothelial Cells: Different Patterns of Response Between Chemokine CX3CL1/CX3CR1 and TNF-α/TNFR1 Signaling Pathways.
Cardiovascular Drugs and Therapy, 2015Co-Authors: Dariusz Szukiewicz, Aleksandra Stangret, Grzegorz Szewczyk, Tarun Kumar Mittal, Malgorzata Wojciechowska, Anna Bilska, Mateusz Watroba, Jan KochanowskiAbstract:Purpose TNF-α induces fractalkine (CX3CL1) and its receptor CX3CR1 in endothelial cells through NF-қB activation. NF-қB inhibitors may reduce the expression of CX3CL1, and modulation of the CX3CL1/CX3CR1 signaling was proposed as a new target for aspirin. We examined the effects of aspirin on CX3CL1 and TNF-α production, as well as CX3CR1 and TNFR1 expression.
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aspirin action in endothelial cells different patterns of response between Chemokine CX3CL1 cx3cr1 and tnf α tnfr1 signaling pathways
Cardiovascular Drugs and Therapy, 2015Co-Authors: Dariusz Szukiewicz, Aleksandra Stangret, Grzegorz Szewczyk, Tarun Kumar Mittal, Malgorzata Wojciechowska, Anna Bilska, Mateusz Watroba, Jan KochanowskiAbstract:Purpose TNF-α induces fractalkine (CX3CL1) and its receptor CX3CR1 in endothelial cells through NF-қB activation. NF-қB inhibitors may reduce the expression of CX3CL1, and modulation of the CX3CL1/CX3CR1 signaling was proposed as a new target for aspirin. We examined the effects of aspirin on CX3CL1 and TNF-α production, as well as CX3CR1 and TNFR1 expression.
Jan Kochanowski - One of the best experts on this subject based on the ideXlab platform.
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Aspirin Action in Endothelial Cells: Different Patterns of Response Between Chemokine CX3CL1/CX3CR1 and TNF-α/TNFR1 Signaling Pathways
Cardiovascular Drugs and Therapy, 2015Co-Authors: Dariusz Szukiewicz, Aleksandra Stangret, Grzegorz Szewczyk, Tarun Kumar Mittal, Malgorzata Wojciechowska, Anna Bilska, Mateusz Watroba, Jan KochanowskiAbstract:Purpose TNF-α induces fractalkine (CX3CL1) and its receptor CX3CR1 in endothelial cells through NF-қB activation. NF-қB inhibitors may reduce the expression of CX3CL1, and modulation of the CX3CL1/CX3CR1 signaling was proposed as a new target for aspirin. We examined the effects of aspirin on CX3CL1 and TNF-α production, as well as CX3CR1 and TNFR1 expression. Methods HUVECs isolated after term pregnancies ( N = 28) were cultured in vitro. Lipopolysaccharide (1 μg/ml) was used as CX3CL1 inducer. HUVECs were exposed to six different concentrations of aspirin (between 1.0 and 6.0 mM) during 7 days. The levels of CX3CL1 and TNF-α in the culture media were measured using ELISA. After termination of the cultures, mean expressions of CX3CR1 and TNFR1 were examined in the immunostained paraffin sections using quantitative immunohistochemistry. Results Aspirin significantly ( p
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Aspirin Action in Endothelial Cells: Different Patterns of Response Between Chemokine CX3CL1/CX3CR1 and TNF-α/TNFR1 Signaling Pathways.
Cardiovascular Drugs and Therapy, 2015Co-Authors: Dariusz Szukiewicz, Aleksandra Stangret, Grzegorz Szewczyk, Tarun Kumar Mittal, Malgorzata Wojciechowska, Anna Bilska, Mateusz Watroba, Jan KochanowskiAbstract:Purpose TNF-α induces fractalkine (CX3CL1) and its receptor CX3CR1 in endothelial cells through NF-қB activation. NF-қB inhibitors may reduce the expression of CX3CL1, and modulation of the CX3CL1/CX3CR1 signaling was proposed as a new target for aspirin. We examined the effects of aspirin on CX3CL1 and TNF-α production, as well as CX3CR1 and TNFR1 expression.
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aspirin action in endothelial cells different patterns of response between Chemokine CX3CL1 cx3cr1 and tnf α tnfr1 signaling pathways
Cardiovascular Drugs and Therapy, 2015Co-Authors: Dariusz Szukiewicz, Aleksandra Stangret, Grzegorz Szewczyk, Tarun Kumar Mittal, Malgorzata Wojciechowska, Anna Bilska, Mateusz Watroba, Jan KochanowskiAbstract:Purpose TNF-α induces fractalkine (CX3CL1) and its receptor CX3CR1 in endothelial cells through NF-қB activation. NF-қB inhibitors may reduce the expression of CX3CL1, and modulation of the CX3CL1/CX3CR1 signaling was proposed as a new target for aspirin. We examined the effects of aspirin on CX3CL1 and TNF-α production, as well as CX3CR1 and TNFR1 expression.
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Chorioamnionitis (ChA) modifies CX3CL1 (fractalkine) production by human amniotic epithelial cells (HAEC) under normoxic and hypoxic conditions
Journal of Inflammation, 2014Co-Authors: Dariusz Szukiewicz, Grzegorz Szewczyk, Michal Pyzlak, Jan Kochanowski, Tarun Kumar Mittal, Krzysztof CendrowskiAbstract:Background Chemokine CX3CL1 possesses unique properties, including combined adhesive and chemotactic functions. Human amniotic epithelial cells (HAEC) show expression of CX3CL1 receptor (CX3CR1) and produce CX3CL1 in response to both physiologic and pathologic stimuli. Chorioamnionitis (ChA) is a common complication of pregnancy and labour. ChA is often accompanied by local hypoxia because of the high oxygen consumption at the site of inflammation. We examined comparatively (ChA-complicated vs. normal pregnancy) CX3CR1 expression and the effects of hypoxia, lipopolysaccharide (LPS), and CX3CR1 blockade on CX3CL1 production in HAEC cultured in vitro. Methods HAEC have been isolated using trypsinization, and cultured under normoxia (20% O_2) vs. hypoxia (5% O_2). According to the experimental design, LPS (1 μg/ml) and neutralizing anti-CX3CR1 antibodies were added at respective time points. Mean CX3CL1 concentration in the supernatant samples were determined by ELISA. Expression of immunostained CX3CR1 was analyzed using quantitative morphometry. Results We have found that the mean levels of CX3CL1 and CX3CR1 expression were remarkably (p
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Fractalkine (CX3CL1) and Its Receptor CX3CR1 May Contribute to Increased Angiogenesis in Diabetic Placenta
Mediators of Inflammation, 2013Co-Authors: Dariusz Szukiewicz, Aleksandra Stangret, Grzegorz Szewczyk, Michal Pyzlak, Jan Kochanowski, Tarun Kumar MittalAbstract:Chemokine CX3CL1 is unique, possessing the ability to act as a dual agent: chemoattractant and adhesive compound. Acting via its sole receptor CX3CR1, CX3CL1 participates in many processes in human placental tissue, including inflammation and angiogenesis. Strongly upregulated by hypoxia and/or inflammation-induced inflammatory cytokines secretion, CX3CL1 may act locally as a key angiogenic factor. Both clinical observations and histopathological studies of the diabetic placenta have confirmed an increased incidence of hypoxia and inflammatory reactions with defective angiogenesis. In this study we examined comparatively (diabetes class C complicated versus normal pregnancy) the correlation between CX3CL1 content in placental tissue, the mean CX3CR1 expression, and density of the network of placental microvessels. A sandwich enzyme immunoassay was applied for CX3CL1 measurement in placental tissue homogenates, whereas quantitative immunohistochemical techniques were used for the assessment of CX3CR1 expression and the microvascular density. Significant differences have been observed for all analyzed parameters between the groups. The mean concentration of CX3CL1 in diabetes was increased and accompanied by augmented placental microvessel density as well as a higher expression of CX3CR1. In conclusion, we suggest involvement of CX3CL1/CX3CR1 signaling pathway in the pathomechanism of placental microvasculature remodeling in diabetes class C.
Jose Maria Parmigianiizquierdo - One of the best experts on this subject based on the ideXlab platform.
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elevated systemic l kynurenine l tryptophan ratio and increased il 1 beta and Chemokine CX3CL1 mcp 1 proinflammatory mediators in patients with long term titanium dental implants
Journal of Clinical Medicine, 2019Co-Authors: Jose Joaquin Merino, Maria Eugenia Cabanamunoz, Adolfo Toledano Gasca, Alba Garcimartin, Juana Benedi, Fabio Camachoalonso, Jose Maria ParmigianiizquierdoAbstract:Titanium is the mean biocompatible metal found in dental titanium alloys (Ti-6Al-4V). The safety of certain dental biomaterial amalgams has been questioned in patients. The levels of several systemic cytokines (interleukin (IL)-1 beta, IL-4: pg/mL) and Chemokines (monocyte chemoattractant protein-1 (MCP-1), soluble fractalkine (CX3CL1: pg/mL) were determined using ELISA and compared between these study groups. The study included 30 controls without dental materials (cont), 57 patients with long-term titanium dental implants plus amalgams (A + I group) as well as 55 patients with long-term dental amalgam alone (A group). All patients (except controls) have had dental titanium implants (Ti-6Al-4V) and/or amalgams for at least 10 years (average: 15 years). We evaluated whether systemic levels of cytokines/Chemokines, kyn/L-trp ratio and aromatic amino acid levels (HPLC: mM/L, Phe, L-Trp, His, Treo) could be altered in patients with long-term dental titanium and/or amalgams. These systemic markers were evaluated in 142 patients. The A + I group had higher L-Kynurenine/L-Tryptophan ratios than patients with long-term dental amalgam fillings alone (A). In addition, levels of IL-1 Beta cytokine, CX3CL1 and MCP-1 Chemokines were higher in the A + I group than in the A group (A). The increased L-kyn/L-trp ratio and MCP-1 and fractalkine receptor (CX3CR1) elevations could suggest enhanced chemotactic responses by these Chemokines in the A + I group.
Grzegorz Szewczyk - One of the best experts on this subject based on the ideXlab platform.
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Anti-inflammatory Action of Metformin with Respect to CX3CL1/CX3CR1 Signaling in Human Placental Circulation in Normal-Glucose Versus High-Glucose Environments
Inflammation, 2018Co-Authors: Dariusz Szukiewicz, Michal Bachanek, Seweryn Trojanowski, Habib Alkhalayla, Aleksandra Stangret, Grzegorz Szewczyk, Michal Pyzlak, Jaroslaw WejmanAbstract:Upregulation of Chemokine CX3CL1 and its receptor CX3CR1 occurs in the diabetic human placenta. Metformin, an insulin-sensitizing biguanide, is used in the therapy of diabetic pregnancy. By preventing the activation of NF-κB, metformin exhibits anti-inflammatory properties. We examined the influence of hyperglycemia (25 mmol/L glucose; HG group; N = 36) on metformin-mediated effects on CX3CL1 and TNF-α production by placental lobules perfused extracorporeally. Additionally, CX3CR1 expression and contents of CX3CR1, TNF-α receptor 1 (TNFR1), and NF-κB proteins in the placental tissue were evaluated. Placentae perfused under normoglycemia (5 mmol/L glucose; NG group; N = 36) served as the control. Metformin (2.5 and 5.0 mg/L; subgroups B and C) lowered the production of CX3CL1 and TNF-α in a dose-dependent and time-dependent manner. Hyperglycemia did not weaken the strength of these metformin effects. Moreover, CX3CL1 levels after perfusion with 5.0 mg/L metformin were reduced by 33.28 and 33.83% (at 120 and 150 min, respectively) in the HG-C subgroup versus 24.98 and 23.66% in the NG-C subgroup, which indicated an augmentation of the metformin action over time in hyperglycemia. CX3CR1 expression was significantly higher in the HG-B and HG-C subgroups compared to that in the NG-B and NG-C subgroups. Increased CX3CR1 protein content in the placental lysates was observed in subgroups B and C. The two higher metformin concentrations significantly decreased the levels of NF-κBp65 protein content in both groups. However, the decrease was significantly stronger in hyperglycemia. TNFR1 upregulation in the HG group was not affected by metformin. Further studies on metformin therapy during pregnancy are needed, including safety issues.
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High Glucose Level Disturbs the Resveratrol-Evoked Curtailment of CX3CL1/CX3CR1 Signaling in Human Placental Circulation.
Mediators of Inflammation, 2017Co-Authors: Dariusz Szukiewicz, Michal Bachanek, Seweryn Trojanowski, Aleksandra Stangret, Grzegorz Szewczyk, Michal Pyzlak, Wojciech Braksator, Jaroslaw WejmanAbstract:Hyperglycemia-induced hyperactivity of Chemokine CX3CL1 (fractalkine) occurs in the human placenta. Anti-inflammatory/antioxidant activities of resveratrol (3,5,4'-trihydroxy-trans-stilbene) are related to the modulation of Chemokine CX3CL1 and its receptor, CX3CR1, signaling pathways. We examined the influence of high glucose (25 mmol/L glucose; HG group; N = 36) on resveratrol-mediated effects on CX3CL1 and TNF-α production by the placental lobule, CX3CR1 expression and contents of CX3CR1, TNF-α receptor 1 (TNFR1), and NF-κB proteins in placental tissue. The placental lobules perfused under normoglycemic conditions formed the control NG group (N = 36). Resveratrol (50 and 100 μM; subgroups B and C) administered into the perfusion fluid lowered the production of both CX3CL1 and TNF-α. The reductions in CX3CL1 levels were more evident in the NG group. CX3CR1 expression was significantly higher in the NG subgroups B and C compared to the HG subgroups B and C (385.2 and 426.5% versus 199.3 and 282.4%, resp.). An increase in CX3CR1 protein content in placental lysates was observed in the NG subgroups B and C. Also, resveratrol significantly decreased NF-κBp65 protein content only in the NG group, not affecting hyperglycemia-elicited TNFR1 upregulation. In conclusion, euglycemia assures optimal effects of resveratrol pertaining to CX3CL1/CX3CR1 signaling in the placenta. Future studies on resveratrol are needed, especially those including maternal-fetal risk assessments.
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Aspirin Action in Endothelial Cells: Different Patterns of Response Between Chemokine CX3CL1/CX3CR1 and TNF-α/TNFR1 Signaling Pathways
Cardiovascular Drugs and Therapy, 2015Co-Authors: Dariusz Szukiewicz, Aleksandra Stangret, Grzegorz Szewczyk, Tarun Kumar Mittal, Malgorzata Wojciechowska, Anna Bilska, Mateusz Watroba, Jan KochanowskiAbstract:Purpose TNF-α induces fractalkine (CX3CL1) and its receptor CX3CR1 in endothelial cells through NF-қB activation. NF-қB inhibitors may reduce the expression of CX3CL1, and modulation of the CX3CL1/CX3CR1 signaling was proposed as a new target for aspirin. We examined the effects of aspirin on CX3CL1 and TNF-α production, as well as CX3CR1 and TNFR1 expression. Methods HUVECs isolated after term pregnancies ( N = 28) were cultured in vitro. Lipopolysaccharide (1 μg/ml) was used as CX3CL1 inducer. HUVECs were exposed to six different concentrations of aspirin (between 1.0 and 6.0 mM) during 7 days. The levels of CX3CL1 and TNF-α in the culture media were measured using ELISA. After termination of the cultures, mean expressions of CX3CR1 and TNFR1 were examined in the immunostained paraffin sections using quantitative immunohistochemistry. Results Aspirin significantly ( p
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Aspirin Action in Endothelial Cells: Different Patterns of Response Between Chemokine CX3CL1/CX3CR1 and TNF-α/TNFR1 Signaling Pathways.
Cardiovascular Drugs and Therapy, 2015Co-Authors: Dariusz Szukiewicz, Aleksandra Stangret, Grzegorz Szewczyk, Tarun Kumar Mittal, Malgorzata Wojciechowska, Anna Bilska, Mateusz Watroba, Jan KochanowskiAbstract:Purpose TNF-α induces fractalkine (CX3CL1) and its receptor CX3CR1 in endothelial cells through NF-қB activation. NF-қB inhibitors may reduce the expression of CX3CL1, and modulation of the CX3CL1/CX3CR1 signaling was proposed as a new target for aspirin. We examined the effects of aspirin on CX3CL1 and TNF-α production, as well as CX3CR1 and TNFR1 expression.
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aspirin action in endothelial cells different patterns of response between Chemokine CX3CL1 cx3cr1 and tnf α tnfr1 signaling pathways
Cardiovascular Drugs and Therapy, 2015Co-Authors: Dariusz Szukiewicz, Aleksandra Stangret, Grzegorz Szewczyk, Tarun Kumar Mittal, Malgorzata Wojciechowska, Anna Bilska, Mateusz Watroba, Jan KochanowskiAbstract:Purpose TNF-α induces fractalkine (CX3CL1) and its receptor CX3CR1 in endothelial cells through NF-қB activation. NF-қB inhibitors may reduce the expression of CX3CL1, and modulation of the CX3CL1/CX3CR1 signaling was proposed as a new target for aspirin. We examined the effects of aspirin on CX3CL1 and TNF-α production, as well as CX3CR1 and TNFR1 expression.
Jose Joaquin Merino - One of the best experts on this subject based on the ideXlab platform.
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elevated systemic l kynurenine l tryptophan ratio and increased il 1 beta and Chemokine CX3CL1 mcp 1 proinflammatory mediators in patients with long term titanium dental implants
Journal of Clinical Medicine, 2019Co-Authors: Jose Joaquin Merino, Maria Eugenia Cabanamunoz, Adolfo Toledano Gasca, Alba Garcimartin, Juana Benedi, Fabio Camachoalonso, Jose Maria ParmigianiizquierdoAbstract:Titanium is the mean biocompatible metal found in dental titanium alloys (Ti-6Al-4V). The safety of certain dental biomaterial amalgams has been questioned in patients. The levels of several systemic cytokines (interleukin (IL)-1 beta, IL-4: pg/mL) and Chemokines (monocyte chemoattractant protein-1 (MCP-1), soluble fractalkine (CX3CL1: pg/mL) were determined using ELISA and compared between these study groups. The study included 30 controls without dental materials (cont), 57 patients with long-term titanium dental implants plus amalgams (A + I group) as well as 55 patients with long-term dental amalgam alone (A group). All patients (except controls) have had dental titanium implants (Ti-6Al-4V) and/or amalgams for at least 10 years (average: 15 years). We evaluated whether systemic levels of cytokines/Chemokines, kyn/L-trp ratio and aromatic amino acid levels (HPLC: mM/L, Phe, L-Trp, His, Treo) could be altered in patients with long-term dental titanium and/or amalgams. These systemic markers were evaluated in 142 patients. The A + I group had higher L-Kynurenine/L-Tryptophan ratios than patients with long-term dental amalgam fillings alone (A). In addition, levels of IL-1 Beta cytokine, CX3CL1 and MCP-1 Chemokines were higher in the A + I group than in the A group (A). The increased L-kyn/L-trp ratio and MCP-1 and fractalkine receptor (CX3CR1) elevations could suggest enhanced chemotactic responses by these Chemokines in the A + I group.