Chlorella vulgaris extract (CVE) was examined for its chelating effects on the myelosuppression induced by lead in Listeria monocytogenes-infected mice. The reduction in the number of bone marrow granulocyte-macrophage progenitors (CFU-GM) observed after the infection was more severe in the groups previously exposed to lead. Extramedullar hematopoiesis, which was drastically increased after the infection, was not altered by the presence of lead. Treatment with CVE, given simultaneously or following lead exposure, restored to control values the myelosuppression observed in infected/lead-exposed mice and produced a significant increase in serum colony-stimulating activity. The benefits of the CVE treatment were also evident in the recovery of thymus weight, since the reduction produced by the infection was further potentiated by lead exposure. The efficacy of CVE was evident when infected and infected/lead-exposed mice were challenged with a lethal dose of L. monocytogenes after a 10-day treatment with 50 mg/kg CVE/day, given simultaneously to the exposure to 1300 ppm lead acetate in drinking water. Survival rates of 30% for the infected group and of 20% for the infected/lead-exposed groups were observed. Evidence that these protective effects of CVE are partly due to its chelating effect was given by the changes observed in blood lead levels. We have observed in the group receiving the CVE/lead simultaneous exposure a dramatic reduction of 66.03% in blood lead levels, when compared to lead-exposed nontreated control. On the other hand, CVE treatment following lead exposure produced a much less effective chelating effect. CVE treatments for 3 or 10 days, starting 24 h following lead exposure, produced a reduction in blood lead levels of 13.5% and 17%, respectively, compared to lead-exposed nontreated controls. The significantly better response observed with the simultaneous CVE/lead administration indicates that the immunomodulation effect of CVE plays an important role in the ability of this algae to reduce blood lead levels. In this regard, additional experiments with gene knockout C57BL/6 mice lacking a functional IFN-gamma gene demonstrated that this cytokine is of paramount importance in the protection afforded by CVE. The antibacterial evaluation measured by the rate of survival demonstrated that, in face of a 100% survival in the control group composed of normal C57BL/6 mice, which are resistant to L. monocytogenes, we observed no protection whatsoever in the IFN-gamma knockout C57BL/6 mice treated with CVE and inoculated with L. monocytogenes.