Research Topics
Genomes and GenesSpecies | J P MizgerdSummaryAffiliation: Harvard University Country: USA Publications
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Publications
Molecular mechanisms of neutrophil recruitment elicited by bacteria in the lungsJoseph 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...- Exon truncation by alternative splicing of murine ICAM-1Joseph 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... - Animal models of human pneumoniaJoseph 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... - Early response cytokines and innate immunity: essential roles for TNF receptor 1 and type I IL-1 receptor during Escherichia coli pneumonia in miceJ 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... - Nuclear factor-kappaB p50 limits inflammation and prevents lung injury during Escherichia coli pneumoniaJoseph 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... 
Lung infection--a public health priorityJoseph P Mizgerd
Harvard School of Public Health, Boston, Massachusetts, USA
PLoS Med 3:e76. 2006- Acute lower respiratory tract infectionJoseph 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 - Roles for early response cytokines during Escherichia coli pneumonia revealed by mice with combined deficiencies of all signaling receptors for TNF and IL-1Joseph 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... - NF-kappaB p50 facilitates neutrophil accumulation during LPS-induced pulmonary inflammationJoseph 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)... - Functions of IkappaB proteins in inflammatory responses to Escherichia coli LPS in mouse lungsJoseph 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... - Lung NF-kappaB activation and neutrophil recruitment require IL-1 and TNF receptor signaling during pneumococcal pneumoniaMatthew 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... - Chronic inflammatory disease alters adhesion molecule requirements for acute neutrophil emigration in mouse skinJ P Mizgerd
Physiology Program, Harvard School of Public Health, Boston, MA 02115, USA
J Immunol 162:5444-8. 1999.... - Roles of tumor necrosis factor receptor signaling during murine Escherichia coli pneumoniaJ 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... - Mechanisms of granulocytosis in the absence of CD18B H Horwitz
Department of Pathology, Brigham and Women s Hospital, Boston, MA 02115, USA
Blood 97:1578-83. 2001.... - Effects of CD18 deficiency on the emigration of murine neutrophils during pneumoniaJ P Mizgerd
Physiology Program, Harvard School of Public Health, Boston, MA 02115, USA
J Immunol 163:995-9. 1999.... - Neutrophil emigration in the skin, lungs, and peritoneum: different requirements for CD11/CD18 revealed by CD18-deficient miceJ 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... - Type I interleukin-1 receptor is required for pulmonary responses to subacute ozone exposure in miceRichard 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... - Mechanisms of the hepatic acute-phase response during bacterial pneumoniaLee 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... - Roles of interleukin-6 in activation of STAT proteins and recruitment of neutrophils during Escherichia coli pneumoniaMatthew 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... - Functions and regulation of NF-kappaB RelA during pneumococcal pneumoniaLee 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... - Alveolar epithelial STAT3, IL-6 family cytokines, and host defense during Escherichia coli pneumoniaLee 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... 
Effect of obesity on pulmonary inflammation induced by acute ozone exposure: role of interleukin-6Jason 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...- CXCR2 is essential for maximal neutrophil recruitment and methacholine responsiveness after ozone exposureRichard 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... - Evaluation of the substrate specificity of human mast cell tryptase beta I and demonstration of its importance in bacterial infections of the lungC 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... - Targeted deletion of tumor suppressor PTEN augments neutrophil function and enhances host defense in neutropenia-associated pneumoniaYitang Li
Department of Pathology, Harvard Medical School, Dana Farber Harvard Cancer Center, Children s Hospital Boston, MA, USA
Blood 113:4930-41. 2009.... - Tumor suppressor PTEN is a physiologic suppressor of chemoattractant-mediated neutrophil functionsKulandayan 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... - Effect of short-term enteral feeding with eicosapentaenoic and gamma-linolenic acids on alveolar macrophage eicosanoid synthesis and bactericidal function in ratsJ D Palombo
Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
Crit Care Med 27:1908-15. 1999.... - Oncostatin M causes eotaxin-1 release from airway smooth muscle: synergy with IL-4 and IL-13Debora 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... - Vascular endothelial growth factor is an important determinant of sepsis morbidity and mortalityKiichiro 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... - Regulation of signal transducer and activator of transcription signaling by the tyrosine phosphatase PTP-BLMasakiyo 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... - Induction of cytoplasmic accumulation of p53: a mechanism for low levels of arsenic exposure to predispose cells for malignant transformationYelin 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... - Cell signaling underlying the pathophysiology of pneumoniaAlice 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... - Competing benefits of tumor necrosis factor-alpha for bacteria and for host defenseJoseph P Mizgerd
Am J Respir Crit Care Med 168:1410-1. 2003 - Very late antigen-4 in CD18-independent neutrophil emigration during acute bacterial pneumonia in miceSadatomo 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 Grants
- 2008 Biology of Acute Respiratory Infections Gordon Research ConferenceJOSEPH 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) ..