Effects of Chlorella vulgaris on bone marrow progenitor cells of mice infected with Listeria monocytogenes.

In this study we investigated the effects of the treatment with Chlorella vulgaris extract (CVE) on the hematopoietic response of granulocyte-macrophage colony-forming unit (CFU-GM) of mice infected with a sublethal dose of Listeria monocytogenes (1 x 10(4) organisms/animal). CVE was given orally as 50 mg/kg/day for 5 days. In the CVE treated/infected groups L. monocytogenes was administered at the end of CVE treatment. The colony stimulating activity of the serum (CSA) was also studied in all groups. Although no effects on CFU-GM, as compared to controls, were observed in the groups receiving CVE alone, the extract produced an increase in CSA levels as compared to controls. On the other hand, the presence of the infection led to a significant reduction in the numbers of CFU-GM as observed at 48 and 72 h after the infection, in spite of the significant increase in serum CSA activity. CVE treatment of infected animals restored the numbers of CFU-GM to control levels. In the treated/ infected group the increased serum CSA was significantly higher than that observed in the only infected group. The CVE treatment (50 and 500 mg/kg) of mice infected with a dose of 3 x 10(5) bacteria/animal, which was lethal for all the non-treated controls, produced a dose-response protection which led to a 20 and 52% survival, respectively. These results demonstrated that CVE produces a significant increase in the resistance of the animals infected with L. monocytogenes, and that this protection is due, at least in part, to increased CFU-GM in the bone marrow of infected animals.

The effects of Chlorella vulgaris in the protection of mice infected with Listeria monocytogenes. Role of natural killer cells.

In this work we have demonstrated the effects of oral administration of Chlorella vulgaris (CV) on Natural Killer cells (NK) activity of mice infected with a sublethal dose of viable Listeria monocytogenes. The treatment with C. vulgaris produced a significant increase on NK cells activity in normal (non-infected) animals compared to the animals that received only vehicle (water) (p < 0.0001). Similarly, the infection alone produced a significant increase on NK cells activity, which was observed at 48 and 72 hours after the inoculation of L. monocytogenes. Moreover, when CV was administered in infected animals, there was an additional increase in NK cells activity which was significantly higher than that found in the infected groups (p < 0.0001). CV treatment (50 and 500mg/Kg) of mice infected with a dose of 3 x 10(5) bacteria/animal, which was lethal for all the non-treated controls, produced a dose-response protection which led to a 20% and 55% survival, respectively (p < 0.0001).

B lymphocytes in mercury-exposed workers.

We have investigated the number of B lymphocytes in mercury-exposed workers. The study group consisted of 33 workers from a mercury-producing plant, mean age 27 years and a mean exposure period 19 months. At the time of testing and for the three previous months, the exposed persons had urinary mercury levels below the currently accepted limit of 50 micrograms g creatinine. A significant reduction in the number of B lymphocytes was observed in the mercury-exposed individuals. We found no correlation between B lymphocytes changes and urinary mercury concentrations, length of exposure or age of the workers.

Immunoglobulin E and autoantibodies in mercury-exposed workers.

In this work we have studied the serum immunoglobulin E (IgE) levels and the concentration of anti-DNA and anti-nucleus antibodies in mercury-exposed workers. The study group consisted of 36 workers from a mercury producing plant, with a mean age of 27 years and a mean exposure period to mercury of 19 months. At the time of testing, and for the three previous months, the exposed population had urinary mercury levels below the currently accept limit of 50 ug/g creatinine. Significantly increased IgE levels was found in the mercury-exposed individuals. Moreover, a moderate negative correlation (r = -0.43 P < 0.05) between the length of exposure to mercury and IgE levels was observed. Anti-DNA and anti-nucleus antibodies were not detected in these workers. These results suggest that the humoral immune response is an indicator of cellular changes in workers chronically exposed to mercury, even in those with urinary mercury concentrations within levels considered safe in the occupational area.

T lymphocytes in mercury-exposed workers.

In this work we have investigated the changes in T-helper and T-suppressor cells and T-cell proliferative response to phytohemagglutinin (PHA) in mercury-exposed workers. The study group consisted of 33 workers from a mercury-producing plant with a mean age of 29 years and a mean exposure period of 19 months. At the time of testing, and for the three previous months, the exposed population had urinary mercury levels below the currently accepted limit of 50 micrograms/g creatinine. A reverse CD4+/CD8+ ratio was observed in the mercury-exposed individuals which was characterized by a reduction in the number of CD4+ lymphocytes. No changes were observed in the proliferative response of lymphocytes from exposed individuals to PHA. Similarly, no proliferative response was observed when lymphocytes from normal individuals were cultivated in the presence of serum from the exposed workers. We found no correlations between lymphocytes changes and urinary mercury concentrations, time of exposure or the age of the workers.

Engulfment and killing capabilities of neutrophils and phagocytic splenic function in persons occupationally exposed to lead.

Phagocytosis and intracellular killing of Candida albicans and Candida pseudotropicalis by neutrophils as well as phagocytic splenic function from lead-exposed workers were studied. Two species of Candida were used since in individuals with myeloperoxidase deficiency neutrophils are unable to kill C. albicans, whereas C. pseudotropicalis can be effectively lysed. Phagocytosis with both antigens and phagocytic splenic function were normal in all the workers studied. However, lytic activity towards C. albicans, but not C. pseudotropicalis was impaired. This defect was observed in lead-exposed workers with blood lead levels and urinary delta-aminolevulinic acid (ALA-U) concentrations in the "safe" (below 60 micrograms/dl and 6 mg/l, respectively) and toxic ranges. An impaired ability to kill C. albicans suggests that lead exposure may lead to a myeloperoxidase deficiency. With the exception of blood lead levels and ALA-U concentrations, there was no correlation between any of the other parameters examined.

Immunoglobulin levels and cellular immune function in lead exposed workers.

The immunological status of lead acid battery workers with blood lead levels and urinary delta-aminolevulinic acid (ALA-U) concentrations ranging from safe to toxic levels has been examined and compared with those of non-exposed, age and sex matched controls. No differences in the serum concentrations of IgG, IgA and IgM between the populations were observed and there existed no correlation between blood lead level or ALA-U concentrations and serum immunoglobulin levels. In addition assessment was made of the capacity of peripheral blood mononuclear cells to respond to the mitogen phytohaemagglutinin (PHA), a correlate of T cell function. As before, there was no difference between exposed and control populations and no correlation between reactivity and blood lead concentration. Our data suggest that chronic exposure to lead fail to compromise lymphocyte function in man.

Immunoglobulin levels in workers exposed to inorganic mercury.

The serum immunoglobulin (IgG, IgM and IgA) concentrations of 44 mercury-exposed workers were examined and compared with those of non-exposed, age- and sex-matched individuals. At the time of testing, the exposed population had a mean (+/- S.D.) mercury urinary concentration of 24.7 +/- 19.1 and in 40 of them urinary mercury levels were below the currently accepted limit of 50 micrograms/g creatinine. Increased IgG, IgA and IgM levels were found in the mercury-exposed individuals and in 16, a second evaluation was performed six months later. During the intervening six months, the level of hygiene was improved throughout the plant, and urinary mercury concentrations were determined monthly in each worker. Despite a significant reduction in mercury urinary concentrations, serum immunoglobulin levels did not return to the normal range. There was no correlation between the length or level of exposure and the immunoglobulin levels. Liver protein synthesis, as studied by factor V, prothrombin time, prealbumin and transaminase activity, was normal and liver injury, as evaluated by serum aspartate and alanine aminotransferase activities (AST and ALT, respectively), was not observed. No haematological abnormalities were noted. These results indicate that "safe" levels of mercury exposure may lead to humoral immunological stimulation.