Concanavalin A-induced resistance to Listeria monocytogenes and activation of macrophages: defect in mice treated with 89Sr.

Abstract

89Sr-treated mice injected with concanavalin A (Con A) 24 h prior to infection with Listeria monocytogenes (LM) could not enhance the clearance of LM from the spleen. Adoptive transfer of normal syngeneic spleen cells together with Con A rendered these animals more resistant. Spleen cells of 89Sr-treated or age-matched control mice were stimulated with con A for 24 h, and supernatant fluids were assessed for macrophage-activating factor (MAF), i.e. the ability to activate resident peritoneal macrophages to kill LM intracellularly in vitro. A defective MAF production by spleen cells was observed in 89Sr-treated, 2 week-old, and athymic nude mice. Also, treatment of spleen cells with anti-Thy-1.2 antiserum plus complement inhibited MAF production. Synergism between spleen cells from 89Sr-treated and nude mice did not occur. The cells required for MAF production were relatively resistant to gamma irradiation. Nylon wool filtration did not modify the ability of spleen cells to make MAF. 89Sr-treated mice possess macrophages responsive to MAF derived from normal spleen cells. The data suggest that the failure of 89Sr-treated mice to develop an anti-LM response observed in thi system could be due to a defective capacity to produce protective humoral factors and/or cells in response to Con A.