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Regulation of eosinophilopoiesis in a murine model of asthma.

Authors
Hogan-MB; Weissman-DN; Hubbs-AF; Gibson-LF; Piktel-D; Landreth-KS
Source
J Immunol 2003 Sep; 171(5):2644-2651
NIOSHTIC No.
20023566
Abstract
Eosinophilic inflammation plays a key role in tissue damage that characterizes asthma. Eosinophils are produced in bone marrow and recent observations in both mice and humans suggest that allergen exposure results in increased output of eosinophils from hemopoietic tissue in individuals with asthma. However, specific mechanisms that alter eosinophilopoiesis in this disease are poorly understood. The current study used a well-characterized murine animal model of asthma to evaluate alterations of eosinophil and eosinophil progenitor cells (CFU-eo) in mice during initial sensitization to allergen and to determine whether observed changes in either cell population were regulated by T lymphocytes. Following the first intranasal installation of OVA, we observed sequential temporal elevation of eosinophils in bone marrow, blood, and lung. In immunocompetent BALB/c mice, elevation of bone marrow eosinophils was accompanied by transient depletion of CFU-eo in that tissue. CFU-eo rebounded to elevated numbers before returning to normal baseline values following intranasal OVA exposure. In T cell-deficient BALB/c nude (BALB/cnu/nu) mice, CFU-eo were markedly elevated following allergen sensitization, in the absence of bone marrow or peripheral blood eosinophilia. These data suggest that eosinophilia of asthma results from alterations in two distinct hemopoietic regulatory mechanisms. Elevation of eosinophil progenitor cells in the bone marrow is T cell independent and likely results from altered bone marrow stromal cell function. Differentiation of eosinophil progenitor cells and phenotypic eosinophilia is T cell dependent and does not occur in athymic nude mice exposed to intranasal allergen.
Keywords
Bronchial-asthma; Models; Bone-marrow; Allergens; Laboratory-animals; Animal-studies; Animals; Lymphocytes; Respiratory-system-disorders; Pulmonary-system-disorders
Contact
Dr. Mary Beth Hogan, Department of Pediatrics, West Virginia University School of Medicine, P.O. Box 9214, Morgantown, WV 26506-9214
CODEN
JOIMA3
Publication Date
20030901
Document Type
Journal Article
Email Address
mhogan@hsc.wvu.edu
Fiscal Year
2003
NTIS Accession No.
NTIS Price
Issue of Publication
5
ISSN
0022-1767
NIOSH Division
HELD
Source Name
The Journal of Immunology
State
WV
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