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From the Departments of Biochemistry and Molecular
Biology*
and Physiology and
Biophysics,
Immunology Research Group,
University of Calgary, Calgary, Alberta, Canada
Eosinophils are usually associated with parasitic and allergic
diseases; however, eosinophilia is also observed in several
types of human tumors, including breast carcinomas. In this
study we examined several human breast carcinoma cell lines for
adhesion molecule expression and the ability to bind and activate
eosinophils. MDA-MB-435S and MDA-MB-468 cells constitutively expressed
both intercellular adhesion molecule-1 (ICAM-1) and vascular cell
adhesion molecule-1 (VCAM-1) and this expression was enhanced by
treatment with tumor necrosis factor-
(TNF-). BT-20 and SK-BR-3
cells only expressed ICAM-1 or VCAM-1 after stimulation with TNF-.
Eosinophils constitutively bound to MDA-MB-435S cells, but not
to BT-20 cells. Stimulation with TNF- slightly enhanced eosinophil
adhesion to MDA-MB-435S cells and dramatically increased adhesion to
BT-20 cells. Greater than 80% of eosinophil adhesion to these cell
lines was blocked with an anti-4-integrin monoclonal antibody. Both
MDA-MB-435S and BT-20 cells also released eosinophil activator(s).
Supernatants from TNF--treated, but not
control-treated, cell lines increased eosinophil adhesion
to fibronectin and increased eosinophil transmigration across
fibronectin-coated transwell plates. Enzyme-linked immunosorbent assays
showed that TNF--stimulated breast carcinoma cells released the
chemokine regulated on activation, T cell expressed and
secreted (RANTES). Addition of an anti-RANTES antibody to breast
carcinoma cell supernatants partially blocked eosinophil activation
suggesting that RANTES in these supernatants was participating in
eosinophil activation. These data show that TNF--stimulated breast
carcinoma cells express mediators that can both bind and activate
eosinophils, suggesting a mechanism for eosinophil localization
to breast carcinoma sites.
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