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Effects of low concentrations of cadmium on immunoglobulin E production by human B lymphocytes in vitro
Sandra Jelovcan1, Andrea Gutschi, Barbara Kleinhappl
1Institute of Hygiene, University of Graz, Universitaetsplatz 4, A-8010, Graz, Austria. sandra.jelovcan@kfunigraz.ac.at
Insights
Cadmium exposure significantly inhibits human immunoglobulin E (IgE) production in B cells. This heavy metal also reduces B cell viability and proliferation, indicating immunotoxic effects.
Area of Science:
- Immunology
- Environmental Health
- Toxicology
Background:
- Cadmium (Cd) exposure can disrupt immune responses, with reported effects ranging from immunosuppression to immunoenhancement.
- Understanding Cd's impact on specific immune components like B lymphocytes is crucial for assessing its health risks.
Purpose of the Study:
- To investigate the effects of cadmium exposure on human immunoglobulin E (IgE) synthesis in B lymphocytes.
- To elucidate the mechanisms underlying cadmium's immunomodulatory actions on B cells.
Main Methods:
- Purified human peripheral blood B lymphocytes were stimulated with IL-4 and anti-human CD40 monoclonal antibody (a-CD40 mAb).
- Exposure to varying concentrations of cadmium (0.1-10 microM) was applied.
- Immunoglobulin production (IgE, IgG, IgM), B cell activation markers (CD69, CD23), viability, and proliferation were assessed.
Main Results:
- Low cadmium concentrations markedly inhibited IgE production in a dose-dependent manner.
- IgG production showed a trend towards enhancement, while IgM levels remained unaffected.
- Cadmium did not impair early B cell activation but reduced viability and proliferation after 24 hours of stimulation.
Conclusions:
- Cadmium exerts immunotoxic effects on human B cells by interfering with initiated cell activation and inducing cytotoxicity.
- The study provides new insights into the immunomodulatory and immunotoxic potential of cadmium on human immune responses, particularly IgE synthesis.
Abstract:
Exposure to cadmium (Cd) can cause a variety of biological effects including alterations of immune responses in animals and humans. Both immunosuppression and immunoenhancement have been reported. The present study was aimed at investigating the consequences of exposure to Cd on the human immunoglobulin (Ig) E synthesis, using purified peripheral blood B lymphocytes and IL-4 and anti-human CD40 monoclonal antibody (a-CD40 mAb) as stimuli. Low concentrations of Cd (0.1-10 microM) markedly inhibited production of IgE in a concentration-dependent manner. IgG production, in contrast to IgE, showed a tendency towards being enhanced by Cd, although with a certain individual variability; IgM production was not affected. Cd failed to alter immediate surface expression of the activation markers CD69 and CD23 indicating that early activation events were not impaired. However, the portion of activated B cells was diminished by Cd after stimulation for more than 24 h, paralleled by a concomitant decrease in viability and a subsequent reduction in proliferation. These data suggest that the mechanism of Cd action on activated B cells involved pathways that interrupted an effectively initiated cell activation and induced a cytotoxic signal. Results from this study thus provide further evidence for and new information on the immunotoxic and immunomodulatory effects of Cd on human immune responses.
