GM-CSF and the impaired pulmonary innate immune response following hyperoxic stress.

GM-CSF and the impaired pulmonary innate immune response following hyperoxic stress. Research Abstract Details 

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GM-CSF and the impaired pulmonary innate immune response following hyperoxic stress. Abstract Text:

Carlos E O Baleeiro,Paul J Christensen,Susan B Morris,Michael P Mendez,Steven E Wilcoxen,Robert Paine,

We have previously demonstrated that mice exposed to sublethal hyperoxia (an atmosphere of >95% oxygen for 4 days, followed by return to room air) have significantly impaired pulmonary innate immune response. Alveolar macrophages (AM) from hyperoxia-exposed mice exhibit significantly diminished antimicrobial activity and markedly reduced production of inflammatory cytokines in response to stimulation with LPS compared with AM from control mice in normoxia. As a consequence of these defects, mice exposed to sublethal hyperoxia are more susceptible to lethal pneumonia with Klebsiella pneumoniae than control mice. Granulocyte/macrophage colony-stimulating factor (GM-CSF) is a growth factor produced by normal pulmonary alveolar epithelial cells that is critically involved in maintenance of normal AM function. We now report that sublethal hyperoxia in vivo leads to greatly reduced alveolar epithelial cell GM-CSF expression. Systemic treatment of mice with recombinant murine GM-CSF during hyperoxia exposure preserved AM function, as indicated by cell surface Toll-like receptor 4 expression and by inflammatory cytokine secretion following stimulation with LPS ex vivo. Treatment of hyperoxic mice with GM-CSF significantly reduced lung bacterial burden following intratracheal inoculation with K. pneumoniae, returning lung bacterial colony-forming units to the level of normoxic controls. These data point to a critical role for continuous GM-CSF activity in the lung in maintenance of normal AM function and demonstrate that lung injury due to hyperoxic stress results in significant impairment in pulmonary innate immunity through suppression of alveolar epithelial cell GM-CSF expression.

GM-CSF and the impaired pulmonary innate immune response following hyperoxic stress. Publishing Authors By Initials

CE Baleeiro,PJ Christensen,SB Morris,MP Mendez,SE Wilcoxen,R Paine,

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GM-CSF and the impaired pulmonary innate immune response following hyperoxic stress. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: American journal of physiology. Lung cellular and

VOLUME: 291

Page Numbers: L1246-55

Journal Abbreviation: Am. J. Physiol. Lung Cell Mol.

ISSN: 1040-0605

DAY: 4

MONTH: 08

YEAR: 2006

GM-CSF and the impaired pulmonary innate immune response following hyperoxic stress. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901229

GM-CSF and the impaired pulmonary innate immune response following hyperoxic stress. Keywords Mesh Terms:

KEYWORDS: Reverse Transcriptase Polymerase Chain R

MESH TERMS: physiopathology

Chemical & Substance for Abstract: GM-CSF and the impaired pulmonary innate immune response following hyperoxic stress. Information

Substance Name: Granulocyte-Macrophage Colony-Stimulatin

Registry Number: 83869-56-1

Grant and Affiliation Information for GM-CSF and the impaired pulmonary innate immune response following hyperoxic stress.

AFFILIATION: Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL-64558

ACRONYM: HL

MEDLINETA: Am J Physiol Lung Cell Mol Phy

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