Mohammed Bourdi

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi Mispairing C57BL/6 substrains of genetically engineered mice and wild-type controls can lead to confounding results as it did in studies of JNK2 in acetaminophen and concanavalin A liver injury
    Mohammed Bourdi
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892 1760, United States
    Chem Res Toxicol 24:794-6. 2011
  2. ncbi Role of IL-6 in an IL-10 and IL-4 double knockout mouse model uniquely susceptible to acetaminophen-induced liver injury
    Mohammed Bourdi
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA
    Chem Res Toxicol 20:208-16. 2007
  3. ncbi Role of interleukin-6 in hepatic heat shock protein expression and protection against acetaminophen-induced liver disease
    Yasuhiro Masubuchi
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, NIH, DHHS, Building 10, Room 8N110, Bethesda, MD 20892 1760, USA
    Biochem Biophys Res Commun 304:207-12. 2003
  4. ncbi Hepatoprotective role of endogenous interleukin-13 in a murine model of acetaminophen-induced liver disease
    Steven B Yee
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA
    Chem Res Toxicol 20:734-44. 2007
  5. ncbi Protective role of Kupffer cells in acetaminophen-induced hepatic injury in mice
    Cynthia Ju
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA
    Chem Res Toxicol 15:1504-13. 2002
  6. ncbi Genomic identification of potential risk factors during acetaminophen-induced liver disease in susceptible and resistant strains of mice
    Kevin D Welch
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA
    Chem Res Toxicol 19:223-33. 2006
  7. ncbi Endogenous interleukin-4 regulates glutathione synthesis following acetaminophen-induced liver injury in mice
    Pauline M Ryan
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, Immunology Center, National Heart, Lung and Blood Institute, National Institutes of Health, 9000 Rockville Pike, Building 10, Room 8N110, Bethesda, Maryland 20892, United States
    Chem Res Toxicol 25:83-93. 2012
  8. ncbi Macrophage migration inhibitory factor in drug-induced liver injury: a role in susceptibility and stress responsiveness
    Mohammed Bourdi
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, 9000 Rockville Pike, Bldg 10, Rm 8N110 Bethesda, MD 20892 1760, USA
    Biochem Biophys Res Commun 294:225-30. 2002
  9. ncbi Protective role of c-Jun N-terminal kinase 2 in acetaminophen-induced liver injury
    Mohammed Bourdi
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892 1760, USA
    Biochem Biophys Res Commun 374:6-10. 2008
  10. ncbi Pathologic role of stressed-induced glucocorticoids in drug-induced liver injury in mice
    Mary Jane Masson
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Biochem Biophys Res Commun 397:453-8. 2010

Collaborators

Detail Information

Publications12

  1. ncbi Mispairing C57BL/6 substrains of genetically engineered mice and wild-type controls can lead to confounding results as it did in studies of JNK2 in acetaminophen and concanavalin A liver injury
    Mohammed Bourdi
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892 1760, United States
    Chem Res Toxicol 24:794-6. 2011
    ..We show here that these mispairings do occur frequently and can lead to inaccurate and conflicting findings...
  2. ncbi Role of IL-6 in an IL-10 and IL-4 double knockout mouse model uniquely susceptible to acetaminophen-induced liver injury
    Mohammed Bourdi
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA
    Chem Res Toxicol 20:208-16. 2007
    ..In conclusion, liver homeostasis following AILD appears to be highly dependent on the activities of both IL-10 and IL-4, which together help prevent overexpression of IL-6 and other potential hepatotoxic factors...
  3. ncbi Role of interleukin-6 in hepatic heat shock protein expression and protection against acetaminophen-induced liver disease
    Yasuhiro Masubuchi
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, NIH, DHHS, Building 10, Room 8N110, Bethesda, MD 20892 1760, USA
    Biochem Biophys Res Commun 304:207-12. 2003
    ..These results suggest that IL-6 and possibly other family members may protect the liver from injury, at least in part, by up-regulating the hepatic expression of several cytoprotective HSPs...
  4. ncbi Hepatoprotective role of endogenous interleukin-13 in a murine model of acetaminophen-induced liver disease
    Steven B Yee
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA
    Chem Res Toxicol 20:734-44. 2007
    ....
  5. ncbi Protective role of Kupffer cells in acetaminophen-induced hepatic injury in mice
    Cynthia Ju
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA
    Chem Res Toxicol 15:1504-13. 2002
    ....
  6. ncbi Genomic identification of potential risk factors during acetaminophen-induced liver disease in susceptible and resistant strains of mice
    Kevin D Welch
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA
    Chem Res Toxicol 19:223-33. 2006
    ..Our findings suggest that comparative gene expression analysis of susceptible and resistant mouse strains may lead to the identification of factors that could have a role in determining the susceptibility of individuals to DILD...
  7. ncbi Endogenous interleukin-4 regulates glutathione synthesis following acetaminophen-induced liver injury in mice
    Pauline M Ryan
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, Immunology Center, National Heart, Lung and Blood Institute, National Institutes of Health, 9000 Rockville Pike, Building 10, Room 8N110, Bethesda, Maryland 20892, United States
    Chem Res Toxicol 25:83-93. 2012
    ....
  8. ncbi Macrophage migration inhibitory factor in drug-induced liver injury: a role in susceptibility and stress responsiveness
    Mohammed Bourdi
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, 9000 Rockville Pike, Bldg 10, Rm 8N110 Bethesda, MD 20892 1760, USA
    Biochem Biophys Res Commun 294:225-30. 2002
    ..These findings support MIF as a critical pro-toxicant signal in drug-induced liver injury with potentially important and novel effects on heat shock protein responsiveness...
  9. ncbi Protective role of c-Jun N-terminal kinase 2 in acetaminophen-induced liver injury
    Mohammed Bourdi
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20892 1760, USA
    Biochem Biophys Res Commun 374:6-10. 2008
    ....
  10. ncbi Pathologic role of stressed-induced glucocorticoids in drug-induced liver injury in mice
    Mary Jane Masson
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA
    Biochem Biophys Res Commun 397:453-8. 2010
    ....
  11. ncbi SIRT3-dependent deacetylation exacerbates acetaminophen hepatotoxicity
    Zhongping Lu
    Center for Molecular Medicine, NHLBI, National Institutes of Health, Building 10 CRC, Room 5 3150, 10 Center Drive, Bethesda, Maryland 20892, USA
    EMBO Rep 12:840-6. 2011
    ..Thus, protein deacetylation enhances xenobiotic liver injury by modulating the binding of a toxic metabolite to mitochondrial proteins...
  12. ncbi Protection against acetaminophen-induced liver injury and lethality by interleukin 10: role of inducible nitric oxide synthase
    Mohammed Bourdi
    Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1760, USA
    Hepatology 35:289-98. 2002
    ..Certain polymorphisms of these factors may have a role in determining the susceptibility of individuals to idiosyncratic DIH...