Adhesion between monocytic and mesothelioma or pleural mesothelial cel
ls influences stromal remodeling in pleural neoplasia. We found that c
ultured monocytic cells (U937) adhere to either human pleural mesothel
ioma (MS-1) or mesothelial (MeT5A) cells in vitro. I-125-fibrinogen bo
und specifically and saturably to either cell line, and specific fibri
nogen binding increased upon stimulation of these cells with proinflam
matory agents such as phorbol myristate (PMA), lipopolysaccharide (LPS
) or tumor necrosis factor (TNF-alpha). We purified the fibrinogen rec
eptor protein from a membrane fraction of MS-1 cells and identified it
by immunoprecipitation as intercellular adhesion molecule (ICAM-1). A
nti-ICAM-1 antibody or antisense oligonucleotides inhibited fibrinogen
-mediated cell adhesion and binding of I-125-fibrinogen to mesotheliom
a or mesothelial cells. Cultured monocytic cells adhere to either meso
thelioma or mesothelial cells, and the interaction is promoted by fibr
inogen binding ICAM-1 at the cell surface. ICAM-1 is expressed by meso
thelioma cells and CD 11b by macrophages in the fibrinous mesothelioma
tumor stroma. The data suggest a common mechanism by which monocytic
cells could adhere to either malignant mesothelioma cells or the mesot
helial surface in pleural neoplasia.