Hartmut Jaeschke

Summary

Affiliation: University of Arizona
Country: USA

Publications

  1. ncbi request reprint Role of reactive oxygen species in hepatic ischemia-reperfusion injury and preconditioning
    Hartmut Jaeschke
    Liver Research Institute and Department of Pharmacology, University of Arizona College of Medicine, AHSC 24136, 1501 N Campbell Avenue, Tucson, AZ 85724, USA
    J Invest Surg 16:127-40. 2003
  2. ncbi request reprint Role of inflammation in the mechanism of acetaminophen-induced hepatotoxicity
    Hartmut Jaeschke
    University of Arizona, Liver Research Institute, College of Medicine, 1501 N Campbell Ave, Tucson, Arizona, AZ 85724, USA
    Expert Opin Drug Metab Toxicol 1:389-97. 2005
  3. ncbi request reprint Intracellular signaling mechanisms of acetaminophen-induced liver cell death
    Hartmut Jaeschke
    Liver Research Institute, University of Arizona, College of Medicine, Tucson, Arizona 85737, USA
    Toxicol Sci 89:31-41. 2006
  4. ncbi request reprint The role of oxidant stress and reactive nitrogen species in acetaminophen hepatotoxicity
    Hartmut Jaeschke
    Liver Research Institute, College of Medicine, University of Arizona, 1501 N Campbell Avenue, Room 6309, Tucson, AZ 85724, USA
    Toxicol Lett 144:279-88. 2003
  5. ncbi request reprint Apoptosis versus oncotic necrosis in hepatic ischemia/reperfusion injury
    Hartmut Jaeschke
    Liver Research Institute, University of Arizona, College of Medicine, Room 6309, 1501 N Campbell Avenue, Tucson, Arizona, USA
    Gastroenterology 125:1246-57. 2003
  6. ncbi request reprint Mechanisms of Liver Injury. II. Mechanisms of neutrophil-induced liver cell injury during hepatic ischemia-reperfusion and other acute inflammatory conditions
    Hartmut Jaeschke
    Liver Research Institute, College of Medicine, University of Arizona, Tucson, 85724, USA
    Am J Physiol Gastrointest Liver Physiol 290:G1083-8. 2006
  7. ncbi request reprint Apoptosis and necrosis in liver disease
    Hartmut Jaeschke
    Liver Research Institute, University of Arizona, Tucson 85724, USA
    Liver Int 24:85-9. 2004
  8. ncbi request reprint Role of caspases in acetaminophen-induced liver injury
    Hartmut Jaeschke
    Liver Research Institute University of Arizona 1501 N Campbell Ave, Room 6309 Tucson, AZ 85724, USA
    Life Sci 78:1670-6. 2006
  9. ncbi request reprint Role of neutrophils in acute inflammatory liver injury
    Hartmut Jaeschke
    Liver Research Institute, University of Arizona, College of Medicine, Tucson, AZ 85737, USA
    Liver Int 26:912-9. 2006
  10. ncbi request reprint Pathophysiological role of the acute inflammatory response during acetaminophen hepatotoxicity
    Cathleen Cover
    Liver Research Institute, University of Arizona, Tucson, AZ 85724, USA
    Toxicol Appl Pharmacol 216:98-107. 2006

Collaborators

Detail Information

Publications57

  1. ncbi request reprint Role of reactive oxygen species in hepatic ischemia-reperfusion injury and preconditioning
    Hartmut Jaeschke
    Liver Research Institute and Department of Pharmacology, University of Arizona College of Medicine, AHSC 24136, 1501 N Campbell Avenue, Tucson, AZ 85724, USA
    J Invest Surg 16:127-40. 2003
  2. ncbi request reprint Role of inflammation in the mechanism of acetaminophen-induced hepatotoxicity
    Hartmut Jaeschke
    University of Arizona, Liver Research Institute, College of Medicine, 1501 N Campbell Ave, Tucson, Arizona, AZ 85724, USA
    Expert Opin Drug Metab Toxicol 1:389-97. 2005
    ....
  3. ncbi request reprint Intracellular signaling mechanisms of acetaminophen-induced liver cell death
    Hartmut Jaeschke
    Liver Research Institute, University of Arizona, College of Medicine, Tucson, Arizona 85737, USA
    Toxicol Sci 89:31-41. 2006
    ....
  4. ncbi request reprint The role of oxidant stress and reactive nitrogen species in acetaminophen hepatotoxicity
    Hartmut Jaeschke
    Liver Research Institute, College of Medicine, University of Arizona, 1501 N Campbell Avenue, Room 6309, Tucson, AZ 85724, USA
    Toxicol Lett 144:279-88. 2003
    ..This concept also reconciles many of the controversial findings of the past and provides a viable hypothesis for the mechanism of hepatocellular injury after AAP overdose...
  5. ncbi request reprint Apoptosis versus oncotic necrosis in hepatic ischemia/reperfusion injury
    Hartmut Jaeschke
    Liver Research Institute, University of Arizona, College of Medicine, Room 6309, 1501 N Campbell Avenue, Tucson, Arizona, USA
    Gastroenterology 125:1246-57. 2003
    ..However, elucidation of critical cell death pathways under clinically relevant conditions will show potentially important therapeutic intervention strategies in hepatic ischemia/reperfusion injury...
  6. ncbi request reprint Mechanisms of Liver Injury. II. Mechanisms of neutrophil-induced liver cell injury during hepatic ischemia-reperfusion and other acute inflammatory conditions
    Hartmut Jaeschke
    Liver Research Institute, College of Medicine, University of Arizona, Tucson, 85724, USA
    Am J Physiol Gastrointest Liver Physiol 290:G1083-8. 2006
    ....
  7. ncbi request reprint Apoptosis and necrosis in liver disease
    Hartmut Jaeschke
    Liver Research Institute, University of Arizona, Tucson 85724, USA
    Liver Int 24:85-9. 2004
    ..In addition, positive controls for the assumed process should be used whenever possible and mechanisms of cell injury should only be investigated in model systems relevant for the human pathophysiology...
  8. ncbi request reprint Role of caspases in acetaminophen-induced liver injury
    Hartmut Jaeschke
    Liver Research Institute University of Arizona 1501 N Campbell Ave, Room 6309 Tucson, AZ 85724, USA
    Life Sci 78:1670-6. 2006
    ....
  9. ncbi request reprint Role of neutrophils in acute inflammatory liver injury
    Hartmut Jaeschke
    Liver Research Institute, University of Arizona, College of Medicine, Tucson, AZ 85737, USA
    Liver Int 26:912-9. 2006
    ....
  10. ncbi request reprint Pathophysiological role of the acute inflammatory response during acetaminophen hepatotoxicity
    Cathleen Cover
    Liver Research Institute, University of Arizona, Tucson, AZ 85724, USA
    Toxicol Appl Pharmacol 216:98-107. 2006
    ..Together, these data do not support the hypothesis that neutrophils aggravate liver injury induced by AAP overdose...
  11. pmc Plasminogen activator inhibitor-1 limits liver injury and facilitates regeneration after acetaminophen overdose
    Mary Lynn Bajt
    Liver Research Institute, University of Arizona, Tucson, Arizona 85724, USA
    Toxicol Sci 104:419-27. 2008
    ..Our data indicate that PAI activation limits liver injury and mortality during APAP hepatotoxicity by preventing excessive hemorrhage and thereby facilitating tissue repair...
  12. ncbi request reprint Pathophysiological role of poly(ADP-ribose) polymerase (PARP) activation during acetaminophen-induced liver cell necrosis in mice
    Cathleen Cover
    Liver Research Institute, University of Arizona, Tucson, Arizona 85737, USA
    Toxicol Sci 84:201-8. 2005
    ..The protection of 3-aminobenzamide against AAP-induced liver injury was due to reduced metabolic activation and potentially its antioxidant effect but independent of PARP-1 inhibition...
  13. ncbi request reprint Reduced inflammatory response and increased microcirculatory disturbances during hepatic ischemia-reperfusion injury in steatotic livers of ob/ob mice
    Tadashi Hasegawa
    Liver Research Institute, College of Medicine, University of Arizona, Tucson, Arizona, USA
    Am J Physiol Gastrointest Liver Physiol 292:G1385-95. 2007
    ..In contrast, the aggravated injury appears to be mediated by ischemic necrosis due to massive impairment of blood and oxygen supply in the steatotic livers...
  14. ncbi request reprint Nuclear translocation of endonuclease G and apoptosis-inducing factor during acetaminophen-induced liver cell injury
    Mary Lynn Bajt
    Liver Research Institute, University of Arizona, College of Medicine, Tucson, Arizona 85724, USA
    Toxicol Sci 94:217-25. 2006
    ....
  15. ncbi request reprint Reduced oncotic necrosis in Fas receptor-deficient C57BL/6J-lpr mice after bile duct ligation
    Jaspreet S Gujral
    Liver Research Institute, University of Arizona, Tucson, AZ 85724, USA
    Hepatology 40:998-1007. 2004
    ..In conclusion, liver injury (oncotic necrosis) after BDL correlated with the severity of the inflammatory response. The minimal amount of apoptosis had no effect on inflammation or on the overall injury...
  16. ncbi request reprint Peroxynitrite-induced mitochondrial and endonuclease-mediated nuclear DNA damage in acetaminophen hepatotoxicity
    Cathleen Cover
    Liver Research Institute, College of Medicine, University of Arizona, Tucson, 85724, USA
    J Pharmacol Exp Ther 315:879-87. 2005
    ..In contrast, nDNA fragmentation after AAP overdose is not caused by caspase-activated DNase but most likely by other intracellular DNase(s), whose activation is dependent on the mitochondrial oxidant stress and peroxynitrite formation...
  17. ncbi request reprint Acetaminophen-induced oxidant stress and cell injury in cultured mouse hepatocytes: protection by N-acetyl cysteine
    Mary Lynn Bajt
    Liver Research Institute, University of Arizona, College of Medicine, Tucson, Arizona 85724, USA
    Toxicol Sci 80:343-9. 2004
    ..Thus, AAP-induced oxidant stress precedes cell necrosis and, in cultured hepatocytes, the oxidant stress is involved in the propagation of cell injury...
  18. ncbi request reprint Generation of hypochlorite-modified proteins by neutrophils during ischemia-reperfusion injury in rat liver: attenuation by ischemic preconditioning
    Tadashi Hasegawa
    Liver Research Institute, University of Arizona, Tucson, AZ 85724, USA
    Am J Physiol Gastrointest Liver Physiol 289:G760-7. 2005
    ..Ischemic preconditioning is an effective intervention for reduction of the overall inflammatory response and, in particular, for limitation of the cytotoxic activity of neutrophils during the later reperfusion period...
  19. ncbi request reprint Role of lipid peroxidation as a mechanism of liver injury after acetaminophen overdose in mice
    Tamara R Knight
    Liver Research Institute, College of Medicine, University of Arizona, Tucson, Arizona 85724, USA
    Toxicol Sci 76:229-36. 2003
    ..Thus, despite the previously shown mitochondrial oxidant stress and peroxynitrite formation, LPO does not appear to be a critical event in AAP-induced hepatotoxicity...
  20. ncbi request reprint Functional importance of ICAM-1 in the mechanism of neutrophil-induced liver injury in bile duct-ligated mice
    Jaspreet S Gujral
    Liver Research Institute, University of Arizona, Tucson, AZ 85724, USA
    Am J Physiol Gastrointest Liver Physiol 286:G499-507. 2004
    ..Thus neutrophils relevant for the aggravation of acute cholestatic liver injury in BDL mice accumulate in hepatic sinusoids, extravasate into the tissue dependent on ICAM-1, and cause cell damage involving reactive oxygen formation...
  21. ncbi request reprint Scavenging peroxynitrite with glutathione promotes regeneration and enhances survival during acetaminophen-induced liver injury in mice
    Mary Lynn Bajt
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, USA
    J Pharmacol Exp Ther 307:67-73. 2003
    ..Treatment with GSH after AAP induced expression of cyclin D1, p21, and PCNA (12-48 h). Thus, GSH treatment after AAP provided long-term hepatoprotection and promotes progression of cell cycle activation in hepatocytes...
  22. ncbi request reprint Mechanisms and pathophysiological implications of sinusoidal endothelial cell gap formation following treatment with galactosamine/endotoxin in mice
    Yoshiya Ito
    Department of Cell Biology and Anatomy, University of Arizona, Tucson, AZ 85724 5044, USA
    Am J Physiol Gastrointest Liver Physiol 291:G211-8. 2006
    ..Although the initial appearance of gap formation is independent of neutrophils, the gaps allow initial contact of neutrophils with damaged hepatocytes. In addition, MMP activation promotes neutrophil accumulation in sinusoids...
  23. ncbi request reprint Innate immunity and acetaminophen-induced liver injury: why so many controversies?
    Hartmut Jaeschke
    Hepatology 48:699-701. 2008
  24. ncbi request reprint Comments on "glycogen synthase kinase-3 mediates acetaminophen-induced apoptosis in human hepatoma cells"
    Hartmut Jaeschke
    J Pharmacol Exp Ther 314:1401-2; author reply 1403-4. 2005
  25. pmc Translocation of iron from lysosomes into mitochondria is a key event during oxidative stress-induced hepatocellular injury
    Akira Uchiyama
    Department of Pharmaceutical and Biomedical Sciences, Medical University of South Carolina, Charleston, SC 29425, USA
    Hepatology 48:1644-54. 2008
    ....
  26. pmc Mitochondrial protein thiol modifications in acetaminophen hepatotoxicity: effect on HMG-CoA synthase
    Kelly K Andringa
    Department of Environmental Health Sciences and The Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL 35294, United States
    Toxicol Lett 177:188-97. 2008
    ..The pathophysiological relevance of these limited changes in protein thiols remains to be investigated...
  27. ncbi request reprint How relevant are neutrophils for acetaminophen hepatotoxicity?
    Hartmut Jaeschke
    Hepatology 43:1191-4. 2006
  28. ncbi request reprint Role of neutrophils in the pathogenesis of acute inflammatory liver injury
    Shashi K Ramaiah
    Department of Pathobiology, College of Veterinary Medicine and Biomedical Sciences, Texas A and M University, College Station, TX 77843 4467, USA
    Toxicol Pathol 35:757-66. 2007
    ..Neutrophil-mediated liver injury has been demonstrated in a variety of diseases and chemical/drug toxicities. Relevant examples are discussed in this review...
  29. ncbi request reprint Mitochondrial bax translocation accelerates DNA fragmentation and cell necrosis in a murine model of acetaminophen hepatotoxicity
    Mary Lynn Bajt
    Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, 3901 Rainbow Blvd, MS 1018, Kansas City, KS 66160, USA
    J Pharmacol Exp Ther 324:8-14. 2008
    ..However, the persistent oxidant stress and peroxynitrite formation in mitochondria may eventually trigger the permeability transition pore opening and release intermembrane proteins independently of Bax...
  30. pmc A new xenobiotic-induced mouse model of sclerosing cholangitis and biliary fibrosis
    Peter Fickert
    Laboratory of Experimental and Molecular Hepatology, Division of Gastroenterology and Hepatology, Department of Medicine, Medical University Graz, Austria
    Am J Pathol 171:525-36. 2007
    ..This model may be valuable to investigate the mechanisms of xenobiotic-induced chronic cholangiopathies and its sequels including biliary fibrosis...
  31. ncbi request reprint Hepatobiliary transporter expression in intercellular adhesion molecule 1 knockout and Fas receptor-deficient mice after common bile duct ligation is independent of the degree of inflammation and oxidative stress
    Martin Wagner
    Laboratory of Experimental and Molecular Hepatology, Division of Gastroenterology and Hepatology, Department of Medicine, Medical University Graz, Auenbruggerplatz 15, A 8036 Graz, Austria
    Drug Metab Dispos 35:1694-9. 2007
    ..Induction of the adaptive transporter response after CBDL is independent of the degree of the inflammatory response. Rather, retention of biliary constituents may determine transporter expression in CBDL...
  32. ncbi request reprint Neutrophil depletion protects against murine acetaminophen hepatotoxicity: another perspective
    Hartmut Jaeschke
    Hepatology 45:1588-9; author reply 1589. 2007
  33. ncbi request reprint Troglitazone hepatotoxicity: are we getting closer to understanding idiosyncratic liver injury?
    Hartmut Jaeschke
    Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, MS 1018, Kansas City, Kansas 66160, USA
    Toxicol Sci 97:1-3. 2007
  34. ncbi request reprint Generation and functional significance of CXC chemokines for neutrophil-induced liver injury during endotoxemia
    Robert B Dorman
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
    Am J Physiol Gastrointest Liver Physiol 288:G880-6. 2005
    ..Thus Gal/ET induced massive, cytokine-dependent CXC chemokine formation in the liver. However, neutrophil extravasation and injury occurred in response to apoptotic cell injury at 6-7 h and was independent of CXC chemokine formation...
  35. ncbi request reprint Involvement of Kupffer cells in the interaction between neutrophils and sinusoidal endothelial cells in rats. Shock 18(2):152-157, 2002
    Hartmut Jaeschke
    Shock 19:394-5; author reply 395-6. 2003
  36. ncbi request reprint Molecular mechanisms of hepatic ischemia-reperfusion injury and preconditioning
    Hartmut Jaeschke
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock 72205, USA
    Am J Physiol Gastrointest Liver Physiol 284:G15-26. 2003
    ..On the basis of current knowledge, preconditioning or pharmacological interventions that mimic these effects have the greatest potential to improve clinical outcome in liver surgery involving ischemic stress and reperfusion...
  37. ncbi request reprint Reactive oxygen as modulator of TNF and fas receptor-mediated apoptosis in vivo: studies with glutathione peroxidase-deficient mice
    Mary Lynn Bajt
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205 7199, USA
    Antioxid Redox Signal 4:733-40. 2002
    ..However, Gpx1 deficiency enhances the susceptibility for secondary necrosis or neutrophil-induced cell injury...
  38. ncbi request reprint Redox considerations in hepatic injury and inflammation
    Hartmut Jaeschke
    Antioxid Redox Signal 4:699-700. 2002
  39. ncbi request reprint Peroxynitrite is a critical mediator of acetaminophen hepatotoxicity in murine livers: protection by glutathione
    Tamara R Knight
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, 4301 W Markham Street, Little Rock, AR 72205, USA
    J Pharmacol Exp Ther 303:468-75. 2002
    ..Delayed GSH treatment enhanced hepatic GSH levels, which scavenged peroxynitrite in a spontaneous reaction. Thus, peroxynitrite is an important mediator of AAP-induced liver cell necrosis...
  40. ncbi request reprint Kupffer cell activation after no-flow ischemia versus hemorrhagic shock
    Hartmut Jaeschke
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock 72205 7199, USA
    Free Radic Biol Med 33:210-9. 2002
    ..Our findings suggest that different therapeutic strategies are necessary to ameliorate the initial injury after low flow ischemia (hemorrhage) compared to cold (transplantation) or warm (Pringle maneuver) no-flow ischemia...
  41. ncbi request reprint Antioxidant gene therapy and hepatic ischemia-reperfusion injury
    Hartmut Jaeschke
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR, USA
    Hepatology 36:243-5. 2002
  42. ncbi request reprint Acetaminophen-induced inhibition of Fas receptor-mediated liver cell apoptosis: mitochondrial dysfunction versus glutathione depletion
    Tamara R Knight
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA
    Toxicol Appl Pharmacol 181:133-41. 2002
    ..Our data suggest that acetaminophen-induced mitochondrial dysfunction and not the initial glutathione depletion is responsible for the interruption of Fas receptor-mediated apoptotic signaling in hepatocytes...
  43. ncbi request reprint Mode of cell death after acetaminophen overdose in mice: apoptosis or oncotic necrosis?
    Jaspreet S Gujral
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, 4301 W Markham St Mailslot 638, Little Rock, AR 72205, USA
    Toxicol Sci 67:322-8. 2002
    ..A similar result was obtained with higher doses of AAP and with the use of fed animals. Thus, oncotic necrosis and not apoptosis is the principal mechanism of liver-cell death after AAP overdose in vivo...
  44. ncbi request reprint Recovery of hepatocellular ATP and "pericentral apoptosis" after hemorrhage and resuscitation
    Markus Paxian
    Department of Anesthesiology and Critical Care Medicine, University of the Saarland, D 66421 Homburg, Germany
    FASEB J 17:993-1002. 2003
    ..quot;..
  45. ncbi request reprint Mechanisms of hepatotoxicity
    Hartmut Jaeschke
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
    Toxicol Sci 65:166-76. 2002
    ..Because of such diverse mechanisms, hepatotoxicity remains a major reason for drug withdrawal from pharmaceutical development and clinical use...
  46. ncbi request reprint Oncotic necrosis and caspase-dependent apoptosis during galactosamine-induced liver injury in rats
    Jaspreet S Gujral
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    Toxicol Appl Pharmacol 190:37-46. 2003
    ..Although some of the apoptotic cells may undergo secondary necrosis, a significant number of hepatocytes die through oncotic necrosis as an independent mechanism of cell death...
  47. ncbi request reprint Mitochondrial permeability transition in acetaminophen-induced necrosis and apoptosis of cultured mouse hepatocytes
    Kazuyoshi Kon
    Department of Cell and Developmental Biology, University of North Carolina at Chapel Hill, 27599 7090, USA
    Hepatology 40:1170-9. 2004
    ..The MPT then induces ATP depletion-dependent necrosis or caspase-dependent apoptosis as determined, in part, by ATP availability from glycolysis...
  48. ncbi request reprint Xanthine oxidase-induced oxidant stress during hepatic ischemia-reperfusion: are we coming full circle after 20 years?
    Hartmut Jaeschke
    Hepatology 36:761-3. 2002
  49. ncbi request reprint Inflammation in response to hepatocellular apoptosis
    Hartmut Jaeschke
    Hepatology 35:964-6. 2002
  50. ncbi request reprint NADPH oxidase-derived oxidant stress is critical for neutrophil cytotoxicity during endotoxemia
    Jaspreet S Gujral
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA
    Am J Physiol Gastrointest Liver Physiol 287:G243-52. 2004
    ..Thus NADPH oxidase could be a promising therapeutic target to prevent neutrophil-mediated liver injury. However, the long-term benefit of this approach needs to be investigated in models relevant for human liver disease...
  51. ncbi request reprint Acetaminophen toxicity in mice lacking NADPH oxidase activity: role of peroxynitrite formation and mitochondrial oxidant stress
    Laura P James
    Department of Pediatrics, University of Arkansas for Medical Sciences, Little Rock, AR, USA
    Free Radic Res 37:1289-97. 2003
    ..These data indicate that superoxide from activated macrophages is not critical to the development of acetaminophen toxicity and provide further support for the role of mitochondrial oxidant stress in acetaminophen toxicity...
  52. ncbi request reprint Gene array analysis of the hepatic response to endotoxin in glutathione peroxidase-deficient mice
    Chengxiu Li
    Inorganic Carcinogenesis Section, Laboratory of Comparative Carcinogenesis NCI at NIEHS, Research Triangle Park, NC 27709, USA
    Toxicol Lett 144:397-406. 2003
    ..Thus, only a combination of gene array analysis with functional studies allows valid conclusions regarding mechanisms of cell injury...
  53. ncbi request reprint Neutrophils aggravate acute liver injury during obstructive cholestasis in bile duct-ligated mice
    Jaspreet S Gujral
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR, USA
    Hepatology 38:355-63. 2003
    ..In conclusion, neutrophils aggravated acute cholestatic liver injury after BDL. This inflammatory injury involves CD18-dependent extravasation of neutrophils from sinusoids and reactive oxygen formation...
  54. ncbi request reprint 24-norUrsodeoxycholic acid is superior to ursodeoxycholic acid in the treatment of sclerosing cholangitis in Mdr2 (Abcb4) knockout mice
    Peter Fickert
    Department of Medicine, Laboratory of Experimental and Molecular Hepatology, Division of Gastroenterology and Hepatology, Medical University Graz, Austria
    Gastroenterology 130:465-81. 2006
    ..Experiments were performed to test in such mice the therapeutic effects of 24-norUrsodeoxycholic acid, a C(23) homologue of ursodeoxycholic acid with 1 fewer methylene group in its side chain...
  55. ncbi request reprint Critical role of CXC chemokines in endotoxemic liver injury in mice
    Hartmut Jaeschke
    J Leukoc Biol 76:1089-90; author reply 1091-2. 2004
  56. ncbi request reprint Neutrophil-mediated tissue injury in alcoholic hepatitis
    Hartmut Jaeschke
    Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, 4301 West Markham Street, Mailslot 638, Little Rock, AR 72205 7199, USA
    Alcohol 27:23-7. 2002
    ..This would allow investigators to test the concept that neutrophils are important for cell injury during alcoholic hepatitis and to identify potential therapeutic intervention strategies...
  57. pmc Lithocholic acid feeding induces segmental bile duct obstruction and destructive cholangitis in mice
    Peter Fickert
    Laboratory of Experimental and Molecular Hepatology, Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University Graz, Auenbruggerplatz 15, A 8036 Graz, Austria
    Am J Pathol 168:410-22. 2006
    ..Thus, we demonstrate that LCA feeding in mice leads to segmental bile duct obstruction, destructive cholangitis, periductal fibrosis, and an adaptive transporter and metabolic enzyme response...