Prolactin enhances production of interferon-γ, interleukin-12, and interleukin-10, but not of tumor necrosis factor-α, in a stimulus-specific manner

Matalka, Khalid Z.

doi:10.1016/s1043-4666(02)00496-9

Cited by 55 publications

(46 citation statements)

References 31 publications

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“…For instance, PRL stimulates inducible NO synthase production, Ig release, and cytokine expression in human leukocytes (7)(8)(9)(10). Furthermore, PRL has anti-apoptotic properties that have been demonstrated in the Nb2 rat lymphoma (11) and in dexamethasone-treated thymocytes (12).…”

mentioning

confidence: 97%

Mechanism of Prostaglandin (PG)E2-Induced Prolactin Expression in Human T Cells: Cooperation of Two PGE2 Receptor Subtypes, E-Prostanoid (EP) 3 and EP4, Via Calcium- and Cyclic Adenosine 5′-Monophosphate-Mediated Signaling Pathways

Gerlo¹,

Verdood²,

Gellersen

et al. 2004

The Journal of Immunology

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We previously reported that prolactin gene expression in the T-leukemic cell line Jurkat is stimulated by PGE2 and that cAMP acts synergistically with Ca2+ or protein kinase C on the activation of the upstream prolactin promoter. Using the transcription inhibitor actinomycin D, we now show that PGE2-induced prolactin expression requires de novo prolactin mRNA synthesis and that PGE2 does not influence prolactin mRNA stability. Furthermore, PGE2-induced prolactin expression was inhibited by protein kinase inhibitor fragment 14–22 and BAPTA-AM, which respectively, inhibit protein kinase A- and Ca2+-mediated signaling cascades. Using specific PGE2 receptor agonists and antagonists, we show that PGE2 induces prolactin expression through engagement of E-prostanoid (EP) 3 and EP4 receptors. We also found that PGE2 induces an increase in intracellular cAMP concentration as well as intracellular calcium concentration via EP4 and EP3 receptors, respectively. In transient transfections, 3000 bp flanking the leukocyte prolactin promoter conferred a weak induction of the luciferase reporter gene by PGE2 and cAMP, whereas cAMP in synergy with ionomycin strongly activated the promoter. Mutation of a C/EBP responsive element at −214 partially abolished the response of the leukocyte prolactin promoter to PGE2, cAMP, and ionomycin plus cAMP.

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mentioning

confidence: 97%

Mechanism of Prostaglandin (PG)E2-Induced Prolactin Expression in Human T Cells: Cooperation of Two PGE2 Receptor Subtypes, E-Prostanoid (EP) 3 and EP4, Via Calcium- and Cyclic Adenosine 5′-Monophosphate-Mediated Signaling Pathways

Gerlo¹,

Verdood²,

Gellersen

et al. 2004

The Journal of Immunology

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“…Prolactin increases the progression of the immune response in autoimmune diseases [7] and stimulates production of cytokines and chemokines, such as TNF-α, IFN-γ, IL-2, IL-10 and IL-12 [8,9]. Serum hyperprolactinemia has been observed in a large number of autoimmune diseases, including CD [10], whereas a reduction in PRL levels detected both in serum from children with multiorgan failure [11] and in PBMs derived from septic hemato-oncological patients [12] correlated with failure of the immune response.…”

mentioning

confidence: 99%

Increased Expression of TLR4 and TLR7 but Not Prolactin mRNA by Peripheral Blood Monocytes in Active Celiac Disease

et al. 2016

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“…The plates were then incubated in 5% CO 2 at 37 ° C for 24 h. After the fi rst incubation, PHA + LPS or only LPS in 40-l volumes was added to give fi nal concentrations of 5 and 1 g/ml for PHA and LPS, respectively, and incubated in 5% CO 2 at 37 ° C for another 24 h [30,31] . Using mixtures of PHA + LPS were found to stimulate both monocytes and T cells by producing higher levels of TNF-␣ and IL-10, but not IL-12, than LPS alone, and in such a system LPS alone did not induce IFN-␥ more than the baseline levels [30,32] . In LPS-stimulated whole blood, monocytes/macrophages are the main inducers of IL-12, TNF-␣ and IL-10 [33] .…”

Section: Whole Blood Culturementioning

confidence: 95%

“…In LPS-stimulated whole blood, monocytes/macrophages are the main inducers of IL-12, TNF-␣ and IL-10 [33] . The results of Maes et al [31] , Matalka [32] and Elenkov et al [33] (and others) indicated that LPS is a T-independent antigen and using PHA + LPS mixtures induces cytokines from both monocytes and T cells. After the second incubation, the blood was collected from wells into sterilized tubes and each well was washed with 0.5 ml of RPMI to ensure removal of the entire well content.…”

Section: Whole Blood Culturementioning

confidence: 99%

Stress-Induced versus Preovulatory and Pregnancy Hormonal Levels in Modulating Cytokine Production following Whole Blood Stimulation

Matalka

Ali²

2005

Neuroimmunomodulation

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Estradiol, progesterone, prolactin and cortisol concentrations are substantially increased during pregnancy. Also, cortisol and prolactin levels are elevated during stress. In the present study, we exposed peripheral blood to estradiol, progesterone, prolactin and cortisol alone or in combination for 24 h before stimulation with T-dependent (phytohemagglutinin, PHA) and independent activators (lipopolysaccharide, LPS) to study their immunomodulatory role in interleukin-12 (IL-12), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), and IL-10 production in a whole blood model. This should be similar to in vivo exposure conditions such as long-term stress, preovulatory or pregnancy periods. The present study showed that the stress-induced and preovulatory levels of prolactin and estradiol, respectively, increased the production of IFN-γ and IL-12 levels (and IL-10 in the case of estradiol) in PHA + LPS-stimulated whole blood, and inhibited a hydrocortisone (100 nmol/l) suppressive effect on IFN-γ, IL-12 and IL-10 productions. In LPS-stimulated whole blood, however, prolactin enhanced only IL-10 production levels in a non-concentration-dependent manner. Higher prolactin levels as in pregnancy did not modulate any of the cytokines, but pregnancy estradiol concentrations only induced higher IL-10 levels in PHA + LPS-stimulated whole blood. All progesterone levels tested revealed no effect on any of the cytokines following whole blood stimulation. Our results indicate that (1) a long exposure time of prolactin and estradiol to whole blood modulates the production of cytokines in a concentration- and stimulus-dependent manner; (2) stress-induced levels of prolactin and preovulatory estradiol concentrations can regulate cortisol-induced cytokine suppression, and (3) even though the cytokine pattern is different, pregnancy estradiol and cortisol levels decreased the IFN-γ/IL-10 ratio, thereby keeping the anti-inflammatory IL-10 levels favored during pregnancy, which could be useful in regulating inflammatory-mediated autoimmune diseases.

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Prolactin enhances production of interferon-γ, interleukin-12, and interleukin-10, but not of tumor necrosis factor-α, in a stimulus-specific manner

Cited by 55 publications

References 31 publications

Mechanism of Prostaglandin (PG)E2-Induced Prolactin Expression in Human T Cells: Cooperation of Two PGE2 Receptor Subtypes, E-Prostanoid (EP) 3 and EP4, Via Calcium- and Cyclic Adenosine 5′-Monophosphate-Mediated Signaling Pathways

Mechanism of Prostaglandin (PG)E2-Induced Prolactin Expression in Human T Cells: Cooperation of Two PGE2 Receptor Subtypes, E-Prostanoid (EP) 3 and EP4, Via Calcium- and Cyclic Adenosine 5′-Monophosphate-Mediated Signaling Pathways

Increased Expression of TLR4 and TLR7 but Not Prolactin mRNA by Peripheral Blood Monocytes in Active Celiac Disease

Stress-Induced versus Preovulatory and Pregnancy Hormonal Levels in Modulating Cytokine Production following Whole Blood Stimulation

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