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Laurence J Britton - One of the best experts on this subject based on the ideXlab platform.
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the role of macrophages in the development of biliary injury in a lipopolysaccharide aggravated hepatic ischaemia reperfusion model
Biochimica et Biophysica Acta, 2017Co-Authors: J Reiling, Kim R Bridle, Frank G Schaap, L Jaskowski, N Santrampurwala, Laurence J Britton, Catherine M Campbell, Peter L M Jansen, S Olde W M Damink, Darrell H G CrawfordAbstract:Abstract Introduction Endotoxins, in the form of lipopolysaccharides (LPS), are potent inducers of biliary injury. However the mechanism by which injury develops remains unclear. We hypothesized that hepatic macrophages are pivotal in the development of endotoxin-induced biliary injury and that no injury would occur in their absence. Material and methods Clodronate liposomes were used to deplete macrophages from the liver. Forty-eight rats were equally divided across six study groups: sham operation (sham), liposome treatment and sham operation (liposomes + sham), 1 mg/kg LPS i.p. (LPS), liposome treatment and LPS administration (liposomes + LPS), hepatic ischaemia-reperfusion injury with LPS administration (IRI + LPS) and liposome treatment followed by IRI + LPS (liposomes + IRI + LPS). Following 6 h of reperfusion, blood, Bile, and liver tissue was collected for further analysis. Small Bile duct injury was assessed, serum liver tests were performed and Bile Composition was evaluated. The permeability of the blood-biliary barrier (BBB) was assessed using intravenously administered horseradish peroxidase (HRP). Results The presence of hepatic macrophages was reduced by 90% in LPS and IRI + LPS groups pre-treated with clodronate liposomes (P Conclusions Depletion of hepatic macrophages did not prevent development of biliary injury following LPS or LPS-enhanced IRI. Cholangiocyte activation rather than macrophage activation may underlie this injury. This article is part of a Special Issue entitled: Cholangiocytes in Health and Diseaseedited by Jesus Banales, Marco Marzioni, Nicholas LaRusso and Peter Jansen.
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low dose lipopolysaccharide causes biliary injury by blood biliary barrier impairment in a rat hepatic ischemia reperfusion model
Liver Transplantation, 2017Co-Authors: J Reiling, Kim R Bridle, Frank G Schaap, L Jaskowski, N Santrampurwala, Marion J J Gijbels, Laurence J BrittonAbstract:This study explored whether bacterial endotoxins, in the form of lipopolysaccharides (LPS), could have an injurious effect on the biliary tract in conjunction with ischemia. A total of 64 rats were randomly assigned to 4 groups: sham operation (sham group), 1 mg/kg LPS intraperitoneal (LPS group), hepatic ischemia/reperfusion (IR; IR group), and IR combined with LPS (IR+LPS group). Following 1 or 6 hours of reperfusion, serum liver tests, Bile duct histology, immunofluorescence microscopy (zonula occludens-1 [ZO-1]), Bile Composition (Bile salts, phospholipids, lactate dehydrogenase), hepatic gene expression (Bile salt transporters and inflammatory mediators), as well as serum and biliary cytokine concentrations were quantified and compared between the study groups. In addition, the integrity of the blood biliary barrier (BBB) was assayed in vivo using horseradish peroxidase (HRP). LPS administration induced severe small Bile duct injury following 6 hours of reperfusion. Furthermore, total Bile salts and bilirubin concentrations in serum were increased in the LPS groups compared with sham controls (LPS, + 3.3-fold and +1.9-fold; IR+LPS, + 3.8-fold and +1.7-fold, respectively). The BBB was impaired in the LPS groups as evidenced by elevated levels of HRP in Bile (+4.9-fold), and decreased expression of claudin 1 (-6.7-fold) and claudin 3 (-3.6-fold). LPS was found to be a potent inducer of small Bile duct injury following hepatic ischemia and 6 hours of reperfusion. This injury was associated with increased permeability of the BBB and impaired hepatic Bile salt clearance. Liver Transplantation 23 194-206 2017 AASLD.
N Santrampurwala - One of the best experts on this subject based on the ideXlab platform.
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the role of macrophages in the development of biliary injury in a lipopolysaccharide aggravated hepatic ischaemia reperfusion model
Biochimica et Biophysica Acta, 2017Co-Authors: J Reiling, Kim R Bridle, Frank G Schaap, L Jaskowski, N Santrampurwala, Laurence J Britton, Catherine M Campbell, Peter L M Jansen, S Olde W M Damink, Darrell H G CrawfordAbstract:Abstract Introduction Endotoxins, in the form of lipopolysaccharides (LPS), are potent inducers of biliary injury. However the mechanism by which injury develops remains unclear. We hypothesized that hepatic macrophages are pivotal in the development of endotoxin-induced biliary injury and that no injury would occur in their absence. Material and methods Clodronate liposomes were used to deplete macrophages from the liver. Forty-eight rats were equally divided across six study groups: sham operation (sham), liposome treatment and sham operation (liposomes + sham), 1 mg/kg LPS i.p. (LPS), liposome treatment and LPS administration (liposomes + LPS), hepatic ischaemia-reperfusion injury with LPS administration (IRI + LPS) and liposome treatment followed by IRI + LPS (liposomes + IRI + LPS). Following 6 h of reperfusion, blood, Bile, and liver tissue was collected for further analysis. Small Bile duct injury was assessed, serum liver tests were performed and Bile Composition was evaluated. The permeability of the blood-biliary barrier (BBB) was assessed using intravenously administered horseradish peroxidase (HRP). Results The presence of hepatic macrophages was reduced by 90% in LPS and IRI + LPS groups pre-treated with clodronate liposomes (P Conclusions Depletion of hepatic macrophages did not prevent development of biliary injury following LPS or LPS-enhanced IRI. Cholangiocyte activation rather than macrophage activation may underlie this injury. This article is part of a Special Issue entitled: Cholangiocytes in Health and Diseaseedited by Jesus Banales, Marco Marzioni, Nicholas LaRusso and Peter Jansen.
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low dose lipopolysaccharide causes biliary injury by blood biliary barrier impairment in a rat hepatic ischemia reperfusion model
Liver Transplantation, 2017Co-Authors: J Reiling, Kim R Bridle, Frank G Schaap, L Jaskowski, N Santrampurwala, Marion J J Gijbels, Laurence J BrittonAbstract:This study explored whether bacterial endotoxins, in the form of lipopolysaccharides (LPS), could have an injurious effect on the biliary tract in conjunction with ischemia. A total of 64 rats were randomly assigned to 4 groups: sham operation (sham group), 1 mg/kg LPS intraperitoneal (LPS group), hepatic ischemia/reperfusion (IR; IR group), and IR combined with LPS (IR+LPS group). Following 1 or 6 hours of reperfusion, serum liver tests, Bile duct histology, immunofluorescence microscopy (zonula occludens-1 [ZO-1]), Bile Composition (Bile salts, phospholipids, lactate dehydrogenase), hepatic gene expression (Bile salt transporters and inflammatory mediators), as well as serum and biliary cytokine concentrations were quantified and compared between the study groups. In addition, the integrity of the blood biliary barrier (BBB) was assayed in vivo using horseradish peroxidase (HRP). LPS administration induced severe small Bile duct injury following 6 hours of reperfusion. Furthermore, total Bile salts and bilirubin concentrations in serum were increased in the LPS groups compared with sham controls (LPS, + 3.3-fold and +1.9-fold; IR+LPS, + 3.8-fold and +1.7-fold, respectively). The BBB was impaired in the LPS groups as evidenced by elevated levels of HRP in Bile (+4.9-fold), and decreased expression of claudin 1 (-6.7-fold) and claudin 3 (-3.6-fold). LPS was found to be a potent inducer of small Bile duct injury following hepatic ischemia and 6 hours of reperfusion. This injury was associated with increased permeability of the BBB and impaired hepatic Bile salt clearance. Liver Transplantation 23 194-206 2017 AASLD.
L Jaskowski - One of the best experts on this subject based on the ideXlab platform.
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the role of macrophages in the development of biliary injury in a lipopolysaccharide aggravated hepatic ischaemia reperfusion model
Biochimica et Biophysica Acta, 2017Co-Authors: J Reiling, Kim R Bridle, Frank G Schaap, L Jaskowski, N Santrampurwala, Laurence J Britton, Catherine M Campbell, Peter L M Jansen, S Olde W M Damink, Darrell H G CrawfordAbstract:Abstract Introduction Endotoxins, in the form of lipopolysaccharides (LPS), are potent inducers of biliary injury. However the mechanism by which injury develops remains unclear. We hypothesized that hepatic macrophages are pivotal in the development of endotoxin-induced biliary injury and that no injury would occur in their absence. Material and methods Clodronate liposomes were used to deplete macrophages from the liver. Forty-eight rats were equally divided across six study groups: sham operation (sham), liposome treatment and sham operation (liposomes + sham), 1 mg/kg LPS i.p. (LPS), liposome treatment and LPS administration (liposomes + LPS), hepatic ischaemia-reperfusion injury with LPS administration (IRI + LPS) and liposome treatment followed by IRI + LPS (liposomes + IRI + LPS). Following 6 h of reperfusion, blood, Bile, and liver tissue was collected for further analysis. Small Bile duct injury was assessed, serum liver tests were performed and Bile Composition was evaluated. The permeability of the blood-biliary barrier (BBB) was assessed using intravenously administered horseradish peroxidase (HRP). Results The presence of hepatic macrophages was reduced by 90% in LPS and IRI + LPS groups pre-treated with clodronate liposomes (P Conclusions Depletion of hepatic macrophages did not prevent development of biliary injury following LPS or LPS-enhanced IRI. Cholangiocyte activation rather than macrophage activation may underlie this injury. This article is part of a Special Issue entitled: Cholangiocytes in Health and Diseaseedited by Jesus Banales, Marco Marzioni, Nicholas LaRusso and Peter Jansen.
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low dose lipopolysaccharide causes biliary injury by blood biliary barrier impairment in a rat hepatic ischemia reperfusion model
Liver Transplantation, 2017Co-Authors: J Reiling, Kim R Bridle, Frank G Schaap, L Jaskowski, N Santrampurwala, Marion J J Gijbels, Laurence J BrittonAbstract:This study explored whether bacterial endotoxins, in the form of lipopolysaccharides (LPS), could have an injurious effect on the biliary tract in conjunction with ischemia. A total of 64 rats were randomly assigned to 4 groups: sham operation (sham group), 1 mg/kg LPS intraperitoneal (LPS group), hepatic ischemia/reperfusion (IR; IR group), and IR combined with LPS (IR+LPS group). Following 1 or 6 hours of reperfusion, serum liver tests, Bile duct histology, immunofluorescence microscopy (zonula occludens-1 [ZO-1]), Bile Composition (Bile salts, phospholipids, lactate dehydrogenase), hepatic gene expression (Bile salt transporters and inflammatory mediators), as well as serum and biliary cytokine concentrations were quantified and compared between the study groups. In addition, the integrity of the blood biliary barrier (BBB) was assayed in vivo using horseradish peroxidase (HRP). LPS administration induced severe small Bile duct injury following 6 hours of reperfusion. Furthermore, total Bile salts and bilirubin concentrations in serum were increased in the LPS groups compared with sham controls (LPS, + 3.3-fold and +1.9-fold; IR+LPS, + 3.8-fold and +1.7-fold, respectively). The BBB was impaired in the LPS groups as evidenced by elevated levels of HRP in Bile (+4.9-fold), and decreased expression of claudin 1 (-6.7-fold) and claudin 3 (-3.6-fold). LPS was found to be a potent inducer of small Bile duct injury following hepatic ischemia and 6 hours of reperfusion. This injury was associated with increased permeability of the BBB and impaired hepatic Bile salt clearance. Liver Transplantation 23 194-206 2017 AASLD.
Kim R Bridle - One of the best experts on this subject based on the ideXlab platform.
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the role of macrophages in the development of biliary injury in a lipopolysaccharide aggravated hepatic ischaemia reperfusion model
Biochimica et Biophysica Acta, 2017Co-Authors: J Reiling, Kim R Bridle, Frank G Schaap, L Jaskowski, N Santrampurwala, Laurence J Britton, Catherine M Campbell, Peter L M Jansen, S Olde W M Damink, Darrell H G CrawfordAbstract:Abstract Introduction Endotoxins, in the form of lipopolysaccharides (LPS), are potent inducers of biliary injury. However the mechanism by which injury develops remains unclear. We hypothesized that hepatic macrophages are pivotal in the development of endotoxin-induced biliary injury and that no injury would occur in their absence. Material and methods Clodronate liposomes were used to deplete macrophages from the liver. Forty-eight rats were equally divided across six study groups: sham operation (sham), liposome treatment and sham operation (liposomes + sham), 1 mg/kg LPS i.p. (LPS), liposome treatment and LPS administration (liposomes + LPS), hepatic ischaemia-reperfusion injury with LPS administration (IRI + LPS) and liposome treatment followed by IRI + LPS (liposomes + IRI + LPS). Following 6 h of reperfusion, blood, Bile, and liver tissue was collected for further analysis. Small Bile duct injury was assessed, serum liver tests were performed and Bile Composition was evaluated. The permeability of the blood-biliary barrier (BBB) was assessed using intravenously administered horseradish peroxidase (HRP). Results The presence of hepatic macrophages was reduced by 90% in LPS and IRI + LPS groups pre-treated with clodronate liposomes (P Conclusions Depletion of hepatic macrophages did not prevent development of biliary injury following LPS or LPS-enhanced IRI. Cholangiocyte activation rather than macrophage activation may underlie this injury. This article is part of a Special Issue entitled: Cholangiocytes in Health and Diseaseedited by Jesus Banales, Marco Marzioni, Nicholas LaRusso and Peter Jansen.
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low dose lipopolysaccharide causes biliary injury by blood biliary barrier impairment in a rat hepatic ischemia reperfusion model
Liver Transplantation, 2017Co-Authors: J Reiling, Kim R Bridle, Frank G Schaap, L Jaskowski, N Santrampurwala, Marion J J Gijbels, Laurence J BrittonAbstract:This study explored whether bacterial endotoxins, in the form of lipopolysaccharides (LPS), could have an injurious effect on the biliary tract in conjunction with ischemia. A total of 64 rats were randomly assigned to 4 groups: sham operation (sham group), 1 mg/kg LPS intraperitoneal (LPS group), hepatic ischemia/reperfusion (IR; IR group), and IR combined with LPS (IR+LPS group). Following 1 or 6 hours of reperfusion, serum liver tests, Bile duct histology, immunofluorescence microscopy (zonula occludens-1 [ZO-1]), Bile Composition (Bile salts, phospholipids, lactate dehydrogenase), hepatic gene expression (Bile salt transporters and inflammatory mediators), as well as serum and biliary cytokine concentrations were quantified and compared between the study groups. In addition, the integrity of the blood biliary barrier (BBB) was assayed in vivo using horseradish peroxidase (HRP). LPS administration induced severe small Bile duct injury following 6 hours of reperfusion. Furthermore, total Bile salts and bilirubin concentrations in serum were increased in the LPS groups compared with sham controls (LPS, + 3.3-fold and +1.9-fold; IR+LPS, + 3.8-fold and +1.7-fold, respectively). The BBB was impaired in the LPS groups as evidenced by elevated levels of HRP in Bile (+4.9-fold), and decreased expression of claudin 1 (-6.7-fold) and claudin 3 (-3.6-fold). LPS was found to be a potent inducer of small Bile duct injury following hepatic ischemia and 6 hours of reperfusion. This injury was associated with increased permeability of the BBB and impaired hepatic Bile salt clearance. Liver Transplantation 23 194-206 2017 AASLD.
J Reiling - One of the best experts on this subject based on the ideXlab platform.
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the role of macrophages in the development of biliary injury in a lipopolysaccharide aggravated hepatic ischaemia reperfusion model
Biochimica et Biophysica Acta, 2017Co-Authors: J Reiling, Kim R Bridle, Frank G Schaap, L Jaskowski, N Santrampurwala, Laurence J Britton, Catherine M Campbell, Peter L M Jansen, S Olde W M Damink, Darrell H G CrawfordAbstract:Abstract Introduction Endotoxins, in the form of lipopolysaccharides (LPS), are potent inducers of biliary injury. However the mechanism by which injury develops remains unclear. We hypothesized that hepatic macrophages are pivotal in the development of endotoxin-induced biliary injury and that no injury would occur in their absence. Material and methods Clodronate liposomes were used to deplete macrophages from the liver. Forty-eight rats were equally divided across six study groups: sham operation (sham), liposome treatment and sham operation (liposomes + sham), 1 mg/kg LPS i.p. (LPS), liposome treatment and LPS administration (liposomes + LPS), hepatic ischaemia-reperfusion injury with LPS administration (IRI + LPS) and liposome treatment followed by IRI + LPS (liposomes + IRI + LPS). Following 6 h of reperfusion, blood, Bile, and liver tissue was collected for further analysis. Small Bile duct injury was assessed, serum liver tests were performed and Bile Composition was evaluated. The permeability of the blood-biliary barrier (BBB) was assessed using intravenously administered horseradish peroxidase (HRP). Results The presence of hepatic macrophages was reduced by 90% in LPS and IRI + LPS groups pre-treated with clodronate liposomes (P Conclusions Depletion of hepatic macrophages did not prevent development of biliary injury following LPS or LPS-enhanced IRI. Cholangiocyte activation rather than macrophage activation may underlie this injury. This article is part of a Special Issue entitled: Cholangiocytes in Health and Diseaseedited by Jesus Banales, Marco Marzioni, Nicholas LaRusso and Peter Jansen.
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low dose lipopolysaccharide causes biliary injury by blood biliary barrier impairment in a rat hepatic ischemia reperfusion model
Liver Transplantation, 2017Co-Authors: J Reiling, Kim R Bridle, Frank G Schaap, L Jaskowski, N Santrampurwala, Marion J J Gijbels, Laurence J BrittonAbstract:This study explored whether bacterial endotoxins, in the form of lipopolysaccharides (LPS), could have an injurious effect on the biliary tract in conjunction with ischemia. A total of 64 rats were randomly assigned to 4 groups: sham operation (sham group), 1 mg/kg LPS intraperitoneal (LPS group), hepatic ischemia/reperfusion (IR; IR group), and IR combined with LPS (IR+LPS group). Following 1 or 6 hours of reperfusion, serum liver tests, Bile duct histology, immunofluorescence microscopy (zonula occludens-1 [ZO-1]), Bile Composition (Bile salts, phospholipids, lactate dehydrogenase), hepatic gene expression (Bile salt transporters and inflammatory mediators), as well as serum and biliary cytokine concentrations were quantified and compared between the study groups. In addition, the integrity of the blood biliary barrier (BBB) was assayed in vivo using horseradish peroxidase (HRP). LPS administration induced severe small Bile duct injury following 6 hours of reperfusion. Furthermore, total Bile salts and bilirubin concentrations in serum were increased in the LPS groups compared with sham controls (LPS, + 3.3-fold and +1.9-fold; IR+LPS, + 3.8-fold and +1.7-fold, respectively). The BBB was impaired in the LPS groups as evidenced by elevated levels of HRP in Bile (+4.9-fold), and decreased expression of claudin 1 (-6.7-fold) and claudin 3 (-3.6-fold). LPS was found to be a potent inducer of small Bile duct injury following hepatic ischemia and 6 hours of reperfusion. This injury was associated with increased permeability of the BBB and impaired hepatic Bile salt clearance. Liver Transplantation 23 194-206 2017 AASLD.