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-Induced Galectin-9
Departments of
* Radiology,
Immunology and Immunopathology,
Perinatology and Gynecology, and
Endocrinology, Kagawa Medical University, Kagawa, Japan;
¶ Department of Vascular Biology, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan; and
|| First Department of Internal Medicine, Kumamoto University School of Medicine, Kumamoto, Japan
Among galectin family members, galectin-9 was first described as a
potent eosinophil chemoattractant derived from Ag-stimulated T cells.
In the present study a role of galectin-9 in the interaction between
eosinophils and fibroblasts was investigated using a human lung
fibroblast cell line, HFL-1. RT-PCR, real-time PCR, and Western blot
analyses revealed that both galectin-9 mRNA and protein in HFL-1 cells
were up-regulated by IFN-
stimulation. On the one hand, IL-4, known
as a Th2 cytokine, did not affect the galectin-9 expression in HFL-1
cells. We further confirmed that IFN- up-regulated the expression of
galectin-9 in primary human dermal fibroblasts. Flow cytometric
analysis revealed that IFN- up-regulated surface galectin-9
expression on HFL-1 cells. Stimulation of HFL-1 cells with IFN-
up-regulated adhesion of eosinophils, but not neutrophils, to HFL-1
cells. This adherence of eosinophils to HFL-1 cells was inhibited by
both lactose and anti-galectin-9 Ab. These findings demonstrate
that IFN--induced galectin-9 expression in fibroblasts mediates
eosinophil adhesion to the cells, suggesting a crucial role of
galectin-9 in IFN--stimulated fibroblasts as a physiological
modulator at the inflammatory sites.
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