Open Access

ARTICLE

Prolactin triggers pro-inflammatory immune responses in peripheral immune cells

Jörg-Matthias Brand, Christoph Frohn, Katharina Cziupka, Christian Brockmann, Holger Kirchner, Jürgen Luhm

Institute of Immunology and Transfusion Medicine, University of Lübeck, Ratzeburger Allee 160, 23538 Lübeck/Germany

* Corresponding Author: Jörg-Matthias Brand,

European Cytokine Network 2004, 15(2), 99-104.

Accepted 06 April 2004;

Abstract

The peptide hormone prolactin (PRL) is produced by specialized cells in the anterior pituitary gland and in a number of sites outside the pituitary. Its biological actions consist of various roles in reproduction, lactation, and of a number of homeostatic biological activities that also include immune functions. Elevated serum PRL concentrations often correlate with abnormalities in immune responses. To determine the influence of PRL on human immune cells, human whole blood cultures were stimulated with lipopolysaccharide (LPS), supple-mented with various concentrations of human recombinant PRL. We found that PRL, at concentrations achievable during pregnancy, anesthesia and medication, significantly amplified interleukin (IL)-12 and tumor necrosis factor-α (TNF-α) synthesis in LPS-stimulated cultures, in a dose-dependent manner. Conversely, synthesis of the anti-inflammatory cytokine IL-10 only increased significantly at very high concentrations of supplemented PRL. PRL alone was not able to induce any measurable secretion of TNF-α, IL-10, or IL-12 in non-stimulated, whole blood cultures. However, we demonstrated that PRL, by itself or in combination with LPS, causes an increase in the binding activity of the transcription factors nuclear factor-κB (NFκB) and interferon regulatory factor-1 (IRF-1), which are known to promote TNF-α and IL-12 secretion. These data suggest that PRL promotes pro-inflammatory immune responses via NFκB and IRF-1, which may affect pathophysiological processes in physiological hyperprolactinemic states.

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