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Updated: Aug 8, 2026

Experimental Infection with Listeria monocytogenes as a Model for Studying Host Interferon-γ Responses
Published on: November 16, 2016
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.
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.

