Intranasal granulocyte-macrophage colony-stimulating factor reduces the Aspergillus burden in an immunosuppressed murine model of pulmonary aspergillosis.

Intranasal granulocyte-macrophage colony-stimulating factor reduces the Aspergillus burden in an immunosuppressed murine model of pulmonary aspergillosis. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Intranasal granulocyte-macrophage colony-stimulating factor reduces the Aspergillus burden in an immunosuppressed murine model of pulmonary aspergillosis. Abstract Text:

Gerardo Quezada,Nadezhda V Koshkina,Patrick Zweidler-McKay,Zichao Zhou,Dimitrios P Kontoyiannis,Eugenie S Kleinerman,Gerardo Quezada,Nadezhda V Koshkina,Patrick Zweidler-McKay,Zichao Zhou,Dimitrios P Kontoyiannis,Eugenie S Kleinerman,

We demonstrated that intranasal granulocyte-macrophage colony-stimulating factor given to immunosuppressed mice infected with pulmonary aspergillosis resulted in a sixfold reduction in the lung fungal burden compared to the result for saline-treated mice (P = 0.045). These data suggest that lung-targeted immunotherapy may be complementary to antifungal agents and may improve patient responses.

Intranasal granulocyte-macrophage colony-stimulating factor reduces the Aspergillus burden in an immunosuppressed murine model of pulmonary aspergillosis. Publishing Authors By Initials

G Quezada,NV Koshkina,P Zweidler-McKay,Z Zhou,DP Kontoyiannis,ES Kleinerman,G Quezada,NV Koshkina,P Zweidler-McKay,Z Zhou,DP Kontoyiannis,ES Kleinerman,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Intranasal granulocyte-macrophage colony-stimulating factor reduces the Aspergillus burden in an immunosuppressed murine model of pulmonary aspergillosis. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Antimicrobial agents and chemotherapy

VOLUME: 52

Page Numbers: 716-8

Journal Abbreviation: Antimicrob. Agents Chemother.

ISSN: 0066-4804

DAY: 5

MONTH: 11

YEAR: 2007

Intranasal granulocyte-macrophage colony-stimulating factor reduces the Aspergillus burden in an immunosuppressed murine model of pulmonary aspergillosis. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 315061

Intranasal granulocyte-macrophage colony-stimulating factor reduces the Aspergillus burden in an immunosuppressed murine model of pulmonary aspergillosis. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Intranasal granulocyte-macrophage colony-stimulating factor reduces the Aspergillus burden in an immunosuppressed murine model of pulmonary aspergillosis. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Intranasal granulocyte-macrophage colony-stimulating factor reduces the Aspergillus burden in an immunosuppressed murine model of pulmonary aspergillosis.

AFFILIATION: Department of Pediatrics, 1515 Holcombe Blvd., Box 87, Houston, TX 77030. ekleiner@mdanderson.org.

Country: United States

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Antimicrob Agents Chemother

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Intranasal granulocyte-macrophage colony-stimulating factor reduces the Aspergillus burden in an immunosuppressed murine model of pulmonary aspergillosis Related Publications

• Bone Marrow Subsets Differentiate into Endothelial Cells and Pericytes Contributing to Ewing's Tumor Vessels.
• Cancer risks following diagnostic and therapeutic radiation exposure in children.
• Cancer screening practices of adult survivors of retinoblastoma at risk of second cancers.
• Corruption of the Fas pathway delays the pulmonary clearance of murine osteosarcoma cells, enhances their metastatic potential, and reduces the effect of aerosol gemcitabine.
• Fas-negative osteosarcoma tumor cells are selected during metastasis to the lungs: the role of the Fas pathway in the metastatic process of osteosarcoma.
• Intranasal granulocyte-macrophage colony-stimulating factor reduces the Aspergillus burden in an immunosuppressed murine model of pulmonary aspergillosis.
• Intratumor murine interleukin-12 gene therapy suppressed the growth of local and distant Ewing's sarcoma.
• Paraquat in the rabbit.
• Pathogenesis of so-called diffuse vascular or collagen disease.
• Some aspects of pulmonary pathology in the Syrian hamster.
• Stromal cell-derived factor-1 stimulates vasculogenesis and enhances Ewing's sarcoma tumor growth in the absence of vascular endothelial growth factor.
• Suppression of Ewing's sarcoma tumor growth, tumor vessel formation, and vasculogenesis following anti vascular endothelial growth factor receptor-2 therapy.
• Targeting Lyn inhibits tumor growth and metastasis in Ewing's sarcoma.
• The Osterix Transcription Factor Down-Regulates Interleukin-1{alpha} Expression in Mouse Osteosarcoma Cells.
• VEGF(165) expression in the tumor microenvironment influences the differentiation of bone marrow-derived pericytes that contribute to the Ewing's sarcoma vasculature.
• VEGF165 is necessary to the metastatic potential of Fas(-) osteosarcoma cells but will not rescue the Fas(+) cells.
• VEGF165, but not VEGF189, Stimulates Vasculogenesis and Bone Marrow Cell Migration into Ewing's Sarcoma Tumors In vivo.