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Prolactin induces enhanced interferon gamma release in peripheral whole blood after stimulation with either PHA or
Tobias Breidthardt1, Christoph Frohn, Jurgen Luhm
1Institute of Immunology and Transfusion Medicine, University of Lübeck School of Medicine, Germany.
Insights
Prolactin significantly boosts interferon-gamma (IFN-gamma) production by immune cells when exposed to common immune stimulants like PHA and LPS. This suggests prolactin plays a key role in modulating the immune response during infections.
Area of Science:
- Immunology
- Neuroendocrinology
- Cell Biology
Background:
- Prolactin is recognized as a crucial mediator in immune-neuroendocrine communication.
- Interferon-gamma (IFN-gamma) is a key cytokine involved in the inflammatory cascade and immune response.
- Understanding prolactin's role in immune cell function is vital for comprehending infection and inflammation.
Purpose of the Study:
- To investigate the effect of human recombinant prolactin on immune cell function.
- To determine if prolactin influences the production of IFN-gamma in response to immune stimuli.
- To explore the potential modulatory role of prolactin in infectious processes.
Main Methods:
- Whole blood assay performed on 15 healthy donors.
- Cell cultures stimulated with phytohemagglutinin (PHA) or lipopolysaccharide (LPS).
- Treatment with varying concentrations of human recombinant prolactin (5-100 ng/ml).
- Quantification of interferon-gamma (IFN-gamma) yields.
Main Results:
- Human recombinant prolactin significantly amplified IFN-gamma yields in response to both PHA and LPS.
- A dose-dependent enhancement of IFN-gamma release was observed in PHA-stimulated cultures.
- Prolactin upregulates IFN-gamma secretion from immune cells in whole blood cultures.
Conclusions:
- Prolactin can modulate IFN-gamma secretion, indicating a role in regulating immune responses to infection.
- Elevated prolactin levels (hyperprolactinemia) may influence inflammatory tissue damage.
- Further research into hyperprolactinemia associated with stress, drugs, or chronic diseases is warranted.
Abstract:
A number of recent studies have demonstrated the importance of prolactin as a key mediator in immune-neuroendocrine communication. Using a whole blood assay and various concentrations of prolactin, we stimulated cell cultures with either the plant lectin PHA or the endotoxin LPS, a widespread agent in common infectious diseases. Studying 15 healthy blood donors we found that human recombinant prolactin, at concentrations from 5 ng/ml to 100 ng/ml, significantly amplified IFN-gamma yields after stimulation with either PHA or LPS. PHA-stimulated cultures revealed a significant dose-dependent enhancement of IFN-gamma release. Our results indicate that prolactin can upregulate IFN-gamma secretion from immune cells in whole blood cell cultures in response to both PHA or LPS. Since IFN-gamma is suspected to play a key role in the cytokine cascade, amplifying the toxic effect of other pro-inflammatory cytokines and ultimately leading to augmented inflammatory tissue damage, our findings point to a modulatory role of prolactin in infection. Special interest should therefore be directed towards any naturally occurring hyperprolactinemia, caused for instance by stress, a number of drugs, and some chronic diseases.
