Early effects of lead on bone marrow cell responsiveness in mice challenged with Listeria monocytogenes.

Listeria monocytogenes challenge of lead-treated mice results in increased mortality. Since macrophage development constitutes the initial phase of the immune response to L. monocytogenes, bone marrow and spleens from Pb-treated mice that were infected with L.

Measurement of macrophage adherence and spreading with weak electric fields.

A new method to monitor macrophage attachment on protein-coated surfaces and spreading in response to activating agents is described. Murine macrophages were cultured on small gold electrodes coated with protein, and attachment and spreading were detected as electrical impedance changes. The rate of attachment of cells to fibronectin-coated electrodes was measured to be significantly greater than to other proteins tested.

Lead-induced alterations of in vitro bone marrow cell responses to colony stimulating factor-1.

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.

Effect of lead on macrophage function.

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).