No abstract

Lead (Pb) has been shown to alter various parameters of immune function such as host resistance and antibody formation. In addition, various heavy metals have been implicated as inducers of autoimmunity. In these experiments, macrophages, isolated from the peritoneal cavity of mice exposed to various doses of lead in vivo as well as cells exposed in vitro were tested for the following immunologic parameters: phagocytosis, antigen presentation, interleukin 1 production, and their ability to stimulate the autologous mixed lymphocyte reaction (AMLR). The results obtained indicate that Pb appears to alter the ability of macrophages to present antigen by enhancing the AMLR while having no effect on phagocytosis or IL-1 production. These data suggest that Pb may interfere with antigen-specific interactions between macrophages and T cells.

Bone marrow cell responsiveness to hematopoietic growth factors is an integral part of immune responsiveness. Since host resistance is often dependent on bone marrow cell responsiveness and Pb alters host resistance, the influence of Pb on bone marrow cell responsiveness to the hematopoietic growth factor CSF-1 was evaluated. Cell number, soft agar colony formation, cell cycle analysis, as well as 3H-thymidine incorporation were utilized to determine if CSF-1 driven bone marrow-derived macrophage (BMDM) proliferation in vitro is altered in the presence of PbCl2. Data obtained indicate that Pb potentiates the ability of CSF-1 to stimulate thymidine incorporation by BMDM; however, colony formation is inhibited reversibly, and the absolute number of cells in culture is adversely affected by Pb. Propagation of BMDM appears to be more sensitive to Pb (100 nM) than other immune parameters. The decrease in bone marrow cell responsiveness to CSF-1 in the presence of Pb observed in this system may contribute to the decrease in host resistance observed in Pb-exposed animals.