Abstract
ICAM-2-deficient mice exhibit prolonged accumulation of eosinophils in lung interstitium concomitant with a delayed increase in eosinophil numbers in the airway lumen during the development of allergic lung inflammation. The ICAM-2-dependent increased and prolonged accumulation of eosinophils in lung interstitium results in prolonged, heightened airway hyperresponsiveness. These findings reveal an essential role for ICAM-2 in the development of the inflammatory and respiratory components of allergic lung disease. This phenotype is caused by the lack of ICAM-2 expression on non-hematopoietic cells. ICAM-2 deficiency on endothelial cells causes reduced eosinophil transmigration in vitro. ICAM-2 is not essential for lymphocyte homing or the development of leukocytes, with the exception of megakaryocyte progenitors, which are significantly reduced.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Administration, Inhalation
-
Animals
-
Bronchial Hyperreactivity / genetics
-
Bronchial Hyperreactivity / immunology
-
Bronchial Hyperreactivity / pathology*
-
Cell Differentiation / genetics
-
Cell Differentiation / immunology
-
Cell Movement / genetics*
-
Cell Movement / immunology
-
Crosses, Genetic
-
Eosinophils / immunology
-
Eosinophils / pathology*
-
Gene Targeting
-
Hematopoietic Stem Cells / pathology
-
Inflammation / genetics
-
Inflammation / immunology
-
Inflammation / pathology
-
Intercellular Adhesion Molecule-1 / genetics*
-
Lymph Nodes / cytology
-
Lymphocyte Count
-
Mice
-
Mice, Inbred AKR
-
Mice, Inbred C57BL
-
Mice, Knockout
-
Ovalbumin / administration & dosage
-
Respiratory Hypersensitivity / genetics
-
Respiratory Hypersensitivity / immunology
-
Respiratory Hypersensitivity / pathology*
-
Sequence Deletion
-
Time Factors
Substances
-
Intercellular Adhesion Molecule-1
-
Ovalbumin