J P Mizgerd

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Molecular mechanisms of neutrophil recruitment elicited by bacteria in the lungs
    Joseph P Mizgerd
    Physiology Program, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA
    Semin Immunol 14:123-32. 2002
  2. ncbi request reprint Exon truncation by alternative splicing of murine ICAM-1
    Joseph P Mizgerd
    Physiology Program, Harvard School of Public Health, Boston, Massachusetts 02115, USA
    Physiol Genomics 12:47-51. 2002
  3. ncbi request reprint Animal models of human pneumonia
    Joseph P Mizgerd
    Molecular and Integerative Physiological Sciences Program, Harvard School of Public Health, Department of Environmental Health, 665 Huntington Ave, Building I Rm 301, Boston, MA 02115, USA
    Am J Physiol Lung Cell Mol Physiol 294:L387-98. 2008
  4. ncbi request reprint Early response cytokines and innate immunity: essential roles for TNF receptor 1 and type I IL-1 receptor during Escherichia coli pneumonia in mice
    J P Mizgerd
    Physiology Program, Harvard School of Public Health, Boston, MA 02115, USA
    J Immunol 166:4042-8. 2001
  5. ncbi request reprint Nuclear factor-kappaB p50 limits inflammation and prevents lung injury during Escherichia coli pneumonia
    Joseph P Mizgerd
    Physiology Program, Harvard School of Public Health, Boston, MA 02115, USA
    Am J Respir Crit Care Med 168:810-7. 2003
  6. pmc Lung infection--a public health priority
    Joseph P Mizgerd
    Harvard School of Public Health, Boston, Massachusetts, USA
    PLoS Med 3:e76. 2006
  7. pmc Acute lower respiratory tract infection
    Joseph P Mizgerd
    Molecular and Integrative Physiological Sciences Program, Harvard School of Public Health, Boston, MA 02115, USA
    N Engl J Med 358:716-27. 2008
  8. ncbi request reprint Roles for early response cytokines during Escherichia coli pneumonia revealed by mice with combined deficiencies of all signaling receptors for TNF and IL-1
    Joseph P Mizgerd
    Physiology Program, Harvard School of Public Health, Harvard Medical School, Boston, MA 02115, USA
    Am J Physiol Lung Cell Mol Physiol 286:L1302-10. 2004
  9. pmc NF-kappaB p50 facilitates neutrophil accumulation during LPS-induced pulmonary inflammation
    Joseph P Mizgerd
    Physiology Program, Harvard School of Public Health, Boston, MA, 02115 USA
    BMC Immunol 5:10. 2004
  10. ncbi request reprint Functions of IkappaB proteins in inflammatory responses to Escherichia coli LPS in mouse lungs
    Joseph P Mizgerd
    Physiology Program, Harvard School of Public Health, Boston, MA 02115, USA
    Am J Respir Cell Mol Biol 27:575-82. 2002

Research Grants

Collaborators

Detail Information

Publications34

  1. ncbi request reprint Molecular mechanisms of neutrophil recruitment elicited by bacteria in the lungs
    Joseph P Mizgerd
    Physiology Program, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA
    Semin Immunol 14:123-32. 2002
    ..The present communication reviews the adhesion molecules, chemokines, other cytokines, and NF- kappa B proteins which regulate the recruitment of neutrophils elicited by bacteria in the lungs...
  2. ncbi request reprint Exon truncation by alternative splicing of murine ICAM-1
    Joseph P Mizgerd
    Physiology Program, Harvard School of Public Health, Boston, Massachusetts 02115, USA
    Physiol Genomics 12:47-51. 2002
    ..Since the affected region is critical for ICAM-1 presentation, dimerization, and solubilization, this alternative splice variant may have unique physiological functions...
  3. ncbi request reprint Animal models of human pneumonia
    Joseph P Mizgerd
    Molecular and Integerative Physiological Sciences Program, Harvard School of Public Health, Department of Environmental Health, 665 Huntington Ave, Building I Rm 301, Boston, MA 02115, USA
    Am J Physiol Lung Cell Mol Physiol 294:L387-98. 2008
    ..Results from studies of pneumonia in animals, combined with complementary basic and translational studies, are elucidating mechanisms responsible for susceptibility to and pathophysiology of lung infection...
  4. ncbi request reprint Early response cytokines and innate immunity: essential roles for TNF receptor 1 and type I IL-1 receptor during Escherichia coli pneumonia in mice
    J P Mizgerd
    Physiology Program, Harvard School of Public Health, Boston, MA 02115, USA
    J Immunol 166:4042-8. 2001
    ..coli in the lungs did not require signaling by either TNFR1 or IL1R1, early response cytokine signaling was critical to KC expression in the pulmonary air spaces and neutrophil emigration from the alveolar septae...
  5. ncbi request reprint Nuclear factor-kappaB p50 limits inflammation and prevents lung injury during Escherichia coli pneumonia
    Joseph P Mizgerd
    Physiology Program, Harvard School of Public Health, Boston, MA 02115, USA
    Am J Respir Crit Care Med 168:810-7. 2003
    ..We interpret these studies to indicate that endogenous p50 protects the host by curbing inflammatory responses to prevent injury, essential to survive pneumonia...
  6. pmc Lung infection--a public health priority
    Joseph P Mizgerd
    Harvard School of Public Health, Boston, Massachusetts, USA
    PLoS Med 3:e76. 2006
  7. pmc Acute lower respiratory tract infection
    Joseph P Mizgerd
    Molecular and Integrative Physiological Sciences Program, Harvard School of Public Health, Boston, MA 02115, USA
    N Engl J Med 358:716-27. 2008
  8. ncbi request reprint Roles for early response cytokines during Escherichia coli pneumonia revealed by mice with combined deficiencies of all signaling receptors for TNF and IL-1
    Joseph P Mizgerd
    Physiology Program, Harvard School of Public Health, Harvard Medical School, Boston, MA 02115, USA
    Am J Physiol Lung Cell Mol Physiol 286:L1302-10. 2004
    ..Thus during E. coli pneumonia in mice, the lack of signaling from TNF-alpha and IL-1 decreases inflammation and preserves lung compliance...
  9. pmc NF-kappaB p50 facilitates neutrophil accumulation during LPS-induced pulmonary inflammation
    Joseph P Mizgerd
    Physiology Program, Harvard School of Public Health, Boston, MA, 02115 USA
    BMC Immunol 5:10. 2004
    ..p50-deficient mice were used to determine how p50 regulates responses to a simpler, non-viable bacterial stimulus in the lungs, E. coli lipopolysaccharide (LPS)...
  10. ncbi request reprint Functions of IkappaB proteins in inflammatory responses to Escherichia coli LPS in mouse lungs
    Joseph P Mizgerd
    Physiology Program, Harvard School of Public Health, Boston, MA 02115, USA
    Am J Respir Cell Mol Biol 27:575-82. 2002
    ..In the absence of IkappaB-beta, IkappaB-alpha or other inhibitory proteins can regulate NF-kappaB functions essential to acute neutrophil emigration in the lungs...
  11. pmc Lung NF-kappaB activation and neutrophil recruitment require IL-1 and TNF receptor signaling during pneumococcal pneumonia
    Matthew R Jones
    Physiology Program, Harvard School of Public Health, Boston, MA 02115, USA
    J Immunol 175:7530-5. 2005
    ..Thus, the combined deficiency of TNF and IL-1 signaling reduces innate immune responses to S. pneumoniae in the lungs, probably due to essential roles for these receptors in activating NF-kappaB...
  12. ncbi request reprint Chronic inflammatory disease alters adhesion molecule requirements for acute neutrophil emigration in mouse skin
    J P Mizgerd
    Physiology Program, Harvard School of Public Health, Boston, MA 02115, USA
    J Immunol 162:5444-8. 1999
    ....
  13. ncbi request reprint Roles of tumor necrosis factor receptor signaling during murine Escherichia coli pneumonia
    J P Mizgerd
    Physiology Program, Harvard School of Public Health, Boston, Massachusetts 02115, USA
    Am J Respir Cell Mol Biol 22:85-91. 2000
    ..During acute E. coli pneumonia, the absence of TNFR signaling compromised bacterial killing, but did not prevent inflammation, as measured by the accumulation of edema fluid and neutrophils...
  14. ncbi request reprint Mechanisms of granulocytosis in the absence of CD18
    B H Horwitz
    Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115, USA
    Blood 97:1578-83. 2001
    ....
  15. ncbi request reprint Effects of CD18 deficiency on the emigration of murine neutrophils during pneumonia
    J P Mizgerd
    Physiology Program, Harvard School of Public Health, Boston, MA 02115, USA
    J Immunol 163:995-9. 1999
    ....
  16. pmc Neutrophil emigration in the skin, lungs, and peritoneum: different requirements for CD11/CD18 revealed by CD18-deficient mice
    J P Mizgerd
    Physiology Program, Harvard School of Public Health, Boston, Massachusetts 02115, USA
    J Exp Med 186:1357-64. 1997
    ..Whereas CD11/CD18 complexes are essential to the dermal emigration of neutrophils during acute dermatitis, CD18-/- mutant mice demonstrate surprising alternative pathways for neutrophil emigration during pneumonia or peritonitis...
  17. pmc Type I interleukin-1 receptor is required for pulmonary responses to subacute ozone exposure in mice
    Richard A Johnston
    Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA
    Am J Respir Cell Mol Biol 37:477-84. 2007
    ..In addition, these results suggest that the induction of IL-6 via IL-1RI may be important in mediating the effects of O(3) during subacute exposure...
  18. pmc Mechanisms of the hepatic acute-phase response during bacterial pneumonia
    Lee J Quinton
    The Pulmonary Center, Boston University School of Medicine, Boston, MA 02118, USA
    Infect Immun 77:2417-26. 2009
    ..These signaling axes may be critical for integrating systemic responses to local infection, balancing antibacterial host defenses and inflammatory injury during acute bacterial pneumonia...
  19. pmc Roles of interleukin-6 in activation of STAT proteins and recruitment of neutrophils during Escherichia coli pneumonia
    Matthew R Jones
    Physiology Program, Harvard School of Public Health, Boston, MA 02115, USA
    J Infect Dis 193:360-9. 2006
    ..coli pneumonia was decreased by IL-6 deficiency. Thus, IL-6 plays essential roles in activating STAT transcription factors, enhancing neutrophil recruitment, and decreasing bacterial burdens during E. coli pneumonia...
  20. pmc Functions and regulation of NF-kappaB RelA during pneumococcal pneumonia
    Lee J Quinton
    Molecular and Integrative Physiological Sciences Program, Harvard School of Public Health, Boston, MA 02115, USA
    J Immunol 178:1896-903. 2007
    ..Our results demonstrate that RelA is essential for the host defense response to pneumococcus in the lungs and that RelA in airway epithelial cells is primarily activated by TNF and IL-1...
  21. pmc Alveolar epithelial STAT3, IL-6 family cytokines, and host defense during Escherichia coli pneumonia
    Lee J Quinton
    Molecular and Integrative Physiological Sciences Program, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115, USA
    Am J Respir Cell Mol Biol 38:699-706. 2008
    ..Together, these results indicate that during E. coli pneumonia, select IL-6 family members activate alveolar epithelial STAT3, which functions to promote neutrophil recruitment and to limit both infection and lung injury...
  22. doi request reprint Effect of obesity on pulmonary inflammation induced by acute ozone exposure: role of interleukin-6
    Jason E Lang
    Molecular and Integrative Physiological Sciences Program, Dept of Environmental Health, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115 6021, USA
    Am J Physiol Lung Cell Mol Physiol 294:L1013-20. 2008
    ..Moreover, obesity-related differences in activation of STAT proteins may contribute to some of the differences in the response of obese vs. lean mice...
  23. ncbi request reprint CXCR2 is essential for maximal neutrophil recruitment and methacholine responsiveness after ozone exposure
    Richard A Johnston
    Physiology Program, Dept of Environmental Health, Harvard School of Public Health, Boston, MA 02115 6021, USA
    Am J Physiol Lung Cell Mol Physiol 288:L61-7. 2005
    ..These results indicate CXCR2 is essential for maximal neutrophil recruitment, epithelial cell sloughing, and persistent increases in MCh responsiveness after an acute O(3) exposure...
  24. ncbi request reprint Evaluation of the substrate specificity of human mast cell tryptase beta I and demonstration of its importance in bacterial infections of the lung
    C Huang
    Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 276:26276-84. 2001
    ..Because neutrophils are required to combat bacterial infections, human tryptase beta I plays a critical role in the antibacterial host defenses of the lung by recruiting neutrophils in a manner that does not alter airway reactivity...
  25. pmc Targeted deletion of tumor suppressor PTEN augments neutrophil function and enhances host defense in neutropenia-associated pneumonia
    Yitang Li
    Department of Pathology, Harvard Medical School, Dana Farber Harvard Cancer Center, Children s Hospital Boston, MA, USA
    Blood 113:4930-41. 2009
    ....
  26. pmc Tumor suppressor PTEN is a physiologic suppressor of chemoattractant-mediated neutrophil functions
    Kulandayan K Subramanian
    Department of Pathology, Harvard Medical School, Boston, MA, USA
    Blood 109:4028-37. 2007
    ..Thus, as a physiologic-negative regulator, PTEN should be a promising therapeutic target for modulating neutrophil functions in various infectious and inflammatory diseases...
  27. ncbi request reprint Effect of short-term enteral feeding with eicosapentaenoic and gamma-linolenic acids on alveolar macrophage eicosanoid synthesis and bactericidal function in rats
    J D Palombo
    Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    Crit Care Med 27:1908-15. 1999
    ....
  28. ncbi request reprint Oncostatin M causes eotaxin-1 release from airway smooth muscle: synergy with IL-4 and IL-13
    Debora S Faffe
    Physiology Program, Harvard School of Public Health, Boston, Mass 02115, USA
    J Allergy Clin Immunol 115:514-20. 2005
    ..Eotaxin is implicated in asthmatic eosinophilia. Oncostatin M (OSM) causes eotaxin release from fibroblasts...
  29. pmc Vascular endothelial growth factor is an important determinant of sepsis morbidity and mortality
    Kiichiro Yano
    Center for Vascular Biology Research, Division of Molecular and Vascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA
    J Exp Med 203:1447-58. 2006
    ..Adenovirus-mediated overexpression of VEGF but not PlGF exacerbated the lipopolysaccharide-mediated toxic effects. Together, these data support a pathophysiological role for VEGF in mediating the sepsis phenotype...
  30. ncbi request reprint Regulation of signal transducer and activator of transcription signaling by the tyrosine phosphatase PTP-BL
    Masakiyo Nakahira
    Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA
    Immunity 26:163-76. 2007
    ..Taken together, our findings demonstrate that PTP-BL is a physiologically important negative regulator of the STAT signaling pathway...
  31. pmc Induction of cytoplasmic accumulation of p53: a mechanism for low levels of arsenic exposure to predispose cells for malignant transformation
    Yelin Huang
    Department of Genetics and Complex Disease, Harvard School of Public Health, Boston, Massachusetts, USA
    Cancer Res 68:9131-6. 2008
    ..Together, our data suggests that arsenic compounds predispose cells to malignant transformation by up-regulation of Hdm2 and subsequent p53 inactivation...
  32. ncbi request reprint Cell signaling underlying the pathophysiology of pneumonia
    Alice S Prince
    Department of Pediatrics and Pharmacology, Columbia University, New York, New York, USA
    Am J Physiol Lung Cell Mol Physiol 291:L297-300. 2006
    ..Also considered were mechanisms of bacterial virulence in the clinical setting (Wiener-Kronish) and the role of alveolar-capillary signaling mechanisms in the initiation of lung inflammation...
  33. ncbi request reprint Competing benefits of tumor necrosis factor-alpha for bacteria and for host defense
    Joseph P Mizgerd
    Am J Respir Crit Care Med 168:1410-1. 2003
  34. ncbi request reprint Very late antigen-4 in CD18-independent neutrophil emigration during acute bacterial pneumonia in mice
    Sadatomo Tasaka
    Division of Integrative Biology, Department of Pediatrics, Rainbow Babies and Children s Hospital and Case Western Reserve University, Cleveland, Ohio 44106, USA
    Am J Respir Crit Care Med 166:53-60. 2002
    ..These data suggest that VLA-4 plays a small role in CD18-independent neutrophil emigration, but the majority of CD18-independent neutrophil emigration induced by bacteria in the lungs occurs through VLA-4-independent mechanisms...

Research Grants3

  1. 2008 Biology of Acute Respiratory Infections Gordon Research Conference
    JOSEPH MIZGERD; Fiscal Year: 2007
    ..The long-term goal is to develop and encourage creative and multidisciplinary investigations discovering innovative and effective prevention and treatment strategies for acute respiratory infections. (End of Abstract) ..