Sialoadhesin expression by bone marrow macrophages derived from Ehrlich-tumor-bearing mice

Sialoadhesin (sheep erythrocyte receptor, SER) is a macrophage-restricted a dhesion molecule that binds certain sialylated ligands. It is borne by bone marrow stromal macrophages, promoting the interaction with developing myel oid cells, and by a subset of tissue macrophages involved in antigen presen tation and activation of tumor-reactive T cells. The expression of sialoadh esin on SER+ macrophages is not constitutive but requires the continuous su pply of a sialoadhesin-inducing serum factor. Tumor growth is often associa ted with marked alterations of myelopoiesis and impairment of T cell activa tion; yet the expression of sialoadhesin in macrophages derived from tumor bearers has not been addressed. Thc aim of this study was to assess whether Ehrlich tumor (ET) - a murine mammary carcinoma growth may modify the sial oadhesin expression by bone marrow macrophages and/or sialoadhesin-inducing activity in ET-bearing sera. Moreover, putative functional sialoadhesin in hibitors produced by ET cells were tested. The results indicate that bone m arrow cells from ET bearers show a seven- to eight-fold decrease in SER+ ce lls as detected by how cytometry. This is accompanied by an overall decreas e in sheep erythrocyte binding to tumor-bearer-derive bone marrow cells, bu t also by lower numbers of plastic-adherent cells. Functional sialoadhesin expression is preserved at the single-cell level and no inhibitors are foun d in ET-bearing sera or ET cell culture supernatants. Tumor progression doe s not impair the sialoadhesin-inducing activity of ET-bearing sera, or the ability of SER- macrophages (e.g. peritoneal macrophages) to respond to suc h an induction. In conclusion, while SER+ macrophages are greatly decreased in bone marrow from ET bearers, this is not due to a down-regulation of si aloadhesin expression, nor to an impairment of sialoadhesin-inducing factor or to the presence of sialoadhesin-binding moieties of tumor origin, but, more likely, to a decrease of fully mature macrophages.