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PubMed2005

Application of sensitive enzymeimmunoassays for oxytocin and prolactin determination in blood plasma of yaks (Poephagus grunniens L.) during milk let down and cyclicity.

Highly sensitive and specific enzymeimmunoassays for oxytocin and prolactin determination in yak plasma using the biotin-streptavidin amplification system and the second antibody coating technique were validated and applied for determining their profiles during milk let down and cyclicity in yaks. Oxytocin EIA was conducted taking duplicate 200 microl of unknown plasma samples and standards per well. The lowest detection limit was 0.2 pg/well, which corresponded to 1pg/ml plasma. Prolactin EIA was carried out directly in 50 microl of yak plasma. The sensitivity of EIA procedure was 5 pg/well prolactin, which corresponded to 0.1 ng/ml plasma. Mean plasma prolactin concentrations although high at estrus were not statistically different (P > 0.05) from the hormone concentrations on other days. Mean plasma prolactin concentrations during non-breeding season were significantly higher (P < 0.001) than that recorded in breeding season. Oxytocin and prolactin profiles were also obtained in two yaks before, during and after milking. A sharp release of oxytocin and prolactin shortly after udder stimulation was observed. High levels of oxytocin and prolactin were maintained during milking, falling sharply thereafter.

Animals↗
PubMed2006

Circadian rhythms of prolactin secretion in neonatal female rabbits after acute separation from their mothers.

Newborn rabbits (Oryctolagus cuniculus) are only nursed for 3-5 min every 24 h and show a circadian increase in activity in anticipation of nursing. The objective of this study was to determine, in neonatal female rabbits after acute separation from the doe for 48 h, the changes in 24-h rhythms of plasma prolactin and median eminence and anterior pituitary concentration of dopamine (DA) and serotonin (5HT). In addition, median eminence concentration of the excitatory amino acid transmitters glutamate (GLU) and aspartate (ASP) and of the inhibitory amino acid transmitters gamma-aminobutyric acid (GABA) and taurine (TAU) was measured. A significant 21% increase of circulating prolactin occurred in isolated pups. In controls pups, plasma prolactin levels showed two peaks, during the first half of the light phase and at the beginning of the scotophase, respectively. In the isolated pups, a phase advance of about 4 h occurred for the two prolactin peaks. Hemicircadian changes of median eminence DA were found in controls, whereas a single daily peak (at 17:00 h) was found in the separated pups. Plasma prolactin and median eminence DA correlated significantly and inversely in the control group only. Pituitary DA content exhibited a single peak in controls and a hemicircadian pattern in isolated pups. Plasma prolactin and pituitary DA correlated significantly in isolated pups only 00000. Pup isolation decreased median eminence 5HT levels, augmented pituitary 5HT levels and disrupted their 24 h rhythmicity. Circulating prolactin correlated inversely with median eminence 5HT and directly with adenohypophysial 5HT only in controls. Isolation of pups generally modified the 24 h pattern of median eminence excitatory and inhibitory amino acid content by causing a prominent decrease at the beginning of the light phase. The results indicate that circadian rhythmicity of prolactin secretory mechanisms in female rabbit pups is significantly affected by pup's isolation from the doe.

Animals↗
PubMed1994

Cervicovaginal prolactin: a marker for spontaneous preterm delivery.

OBJECTIVE: Our purpose was to determine whether the presence of prolactin in cervicovaginal washings is associated with preterm birth. STUDY DESIGN: A cohort of 80 patients underwent a washing of the ectocervix and vaginal fornices with a normal saline solution. The cohort consisted of two groups: 40 inpatients requiring tocolysis and 40 asymptomatic outpatients. The saline solution aspirates were centrifuged, the supernatant was stored at -70 degrees C, and a radioimmunoassay for prolactin was run in batch fashion. A prolactin concentration greater than the detection limit of the assay was considered a positive test result. RESULTS: Prolactin was identified in significantly more symptomatic patients than asymptomatic controls (50% vs 5%, p < 0.0001). In symptomatic patients cervicovaginal prolactin had an 80% positive predictive value and a 65% negative predictive value for delivery at < or = 34 weeks' gestation. Patients testing positive for prolactin had significantly shorter latency from testing to delivery (16 +/- 17 vs 34 +/- 24 days, p = 0.02) and had significantly lower birth weights (1985 +/- 729 vs 2583 +/- 696 gm, p = 0.01) compared with patients testing negative. Prolactin was also identified in two asymptomatic patients, both of whom were delivered before term. CONCLUSIONS: Cervicovaginal prolactin is a biochemical marker for preterm delivery, a shorter latency period to delivery, and lower birth weight in symptomatic patients. This test may also prove to be a valuable marker for preterm birth in asymptomatic women.

Adult↗
PubMed1988

Human uterine luminal fluid volumes and prolactin levels in normal menstrual cycles.

Human uterine luminal fluid has not been well characterized. Prolactin is produced in vitro by decidualized human endometrium and is secreted in vivo into the uterine luminal fluid of cynomolgus monkeys. Uterine luminal fluid prolactin has not been demonstrated in vivo in human beings. To study cyclic uterine luminal fluid volumes and prolactin levels, uterine luminal fluid was aspirated 8 to 13 times each during a single menstrual cycle in six ovulatory women. No anesthesia was used. Seventy of 75 (93%) attempts were successful; there were no complications. Serum estradiol, progesterone, luteinizing hormone, and prolactin levels were assayed every 1 to 3 days. Uterine luminal fluid volume and prolactin were normalized to the luteinizing hormone peak (day 0). Uterine luminal fluid volumes were relatively constant until the early luteal phase, when they then decreased. Uterine luminal fluid prolactin was detectable in all samples. Mean values were stable until day +3 or +4, after which they rose to a peak at day +9 or +10. This study establishes that (1) frequent uterine luminal fluid sampling is possible; (2) uterine luminal fluid volume decreases in the luteal phase; (3) uterine luminal fluid prolactin is detectable in vivo in women and its concentration increases in the luteal phase; and (4) cyclic human uterine luminal fluid prolactin levels differ from those in cynomolgus monkeys and from those anticipated from human in vitro studies.

Blood↗
PubMed2000

Establishment of plasma membrane polarity in mammary epithelial cells correlates with changes in prolactin trafficking and in annexin VI recruitment to membranes.

Mammary epithelial cells (MEC) of lactating animals ferry large amounts of milk constituents in vesicular structures which have mostly been characterized by morphological approaches (Ollivier-Bousquet, 1998). Recently, we have shown that under conditions of lipid deprivation, perturbed prolactin traffic paralleled changes in the membrane phospholipid composition and in the cytosol versus membrane distribution of annexin VI (Ollivier-Bousquet et al., 1997). To obtain additional information on the membrane events involved in the vesicular transport of the hormone to the apical pole of the cell, we conducted a biochemical study on prolactin-containing vesicles in MEC at two different stages of differentiation. We first showed that MEC of pregnant and lactating rabbits exhibited membrane characteristics of non-polarized and polarized cells respectively, using annexin IV and the alpha-6 subunit of integrin as membrane markers. Incubation of both cell types with biotinylated prolactin for 1 h at 15 degrees C, followed by a 10-min chase at 37 degrees C revealed that prolactin transport was activated upon MEC membrane polarization. This was confirmed by subcellular fractionation of prolactin-containing vesicles on discontinuous density gradients. In non-polarized MEC, (125)I-prolactin was mainly recovered in gradient fractions enriched with endocytotic vesicles either after incubation at 15 degrees C or after a 10-min chase at 37 degrees C. In contrast, in polarized MEC, the hormone switched from endocytotic compartments to a fraction enriched in exocytotic clathrin-coated vesicles during the 10-min chase at 37 degrees C. Association of annexin VI to prolactin carriers was next studied in both non-polarized and polarized cells. Membrane compartments collected at each gradient interface were solubilized under mild conditions by Triton X-100 (TX100) and the distribution of annexin VI in TX100-insoluble and TX100-soluble fractions was analyzed by Western blotting. Upon MEC polarization, the amount of annexin VI recovered in TX100-insoluble fractions changed. Quite interestingly, it increased in a membrane fraction enriched with endocytotic clathrin-coated vesicles, suggesting that annexin VI may act as a sorting signal in prolactin transport.

Animals↗
PubMed1999

Salivary prolactin as a marker for central serotonin turnover.

Central nervous system (CNS) serotonin deficits have been linked to many pathological behaviors in both human and nonhuman primates. The plasma prolactin response to fenfluramine has been widely used to assess CNS serotonin functioning in humans. Prolactin is also found as an integrated measure in saliva. We hypothesized that salivary prolactin concentrations would correlate positively with cerebrospinal fluid (CSF) 5-hydroxyindoleacetic acid (5-HIAA) in rhesus monkeys. Twenty-seven adult male and female rhesus macaques (Macaca mulatta) were sampled for concurrent saliva, blood, and CSF. Saliva and blood serum were assayed for prolactin concentrations, and CSF was assayed for 5-HIAA, homovanillic acid (HVA), and 3-methoxy-4-hydroxyphenylglycol (MHPG). Salivary prolactin concentrations were positively correlated with CSF 5-HIAA concentrations. No other relationships between any of the measures, including that between salivary prolactin and serum prolactin, were found to be statistically significant. These findings suggest the possibility of using salivary prolactin concentrations as an index of CNS serotonin turnover in humans.

Animals↗
PubMed1989

Changes in plasma and pituitary levels of prolactin in the toad, Bufo japonicus, throughout the year with special reference to the breeding migration.

Monthly surveys of the plasma prolactin level in Bufo japonicus at two localities, one in Tokyo and the other in Saitama Prefecture, revealed that the level was highest during the month of breeding in early spring with an additional peak recognized in autumn. The level was lowest during the winter torpid period before breeding and during the spring torpid period after breeding. The pituitary prolactin content observed in Tokyo also showed an annual cycle similar to the plasma prolactin, except that the content in winter was higher than that in summer. A further precise survey of the plasma prolactin level before and during the breeding period revealed that the level in male toads migrating toward the pond for breeding was as low as the level in torpid toads, and also that the level was elevated in only about 50% of migrating female toads. In the pond, almost all female and male toads showed high plasma prolactin levels. Soon after the females finished breeding and returned to land, the level declined to the baseline without exception. In contrast, many males retained high levels on land. The present results indicate that prolactin is not a water drive factor, at least in B. japonicus. Prolactin may, however, play a role in toad osmoregulation in water. There is a possibility that the high prolactin level in some of the migrating female toads is related to oviductal secretion, as some female toads ovulate during migration.

Acclimatization↗
PubMed1985

Decreased prolactin secretion in childhood obesity.

Twelve obese patients and 7 control subjects, age and sex matched, whose weights were greater than 200% of ideal weight and 100% of ideal body weight, respectively, underwent intravenous insulin and thyroid releasing hormone (TRH) tests. Serial prolactin growth hormone, insulin, blood sugar, cortisol, glucagon, thyrotropin stimulating hormone, thyroxine, and triiodothyronine were obtained by RIA. Obese patients showed no significant differences from controls in basal and nadir glucose, basal and peak glucagon, cortisol, and thyroid responses to both tests. Basal insulin levels were higher (36 +/- 9.4 vs 10 +/- 2.3 microU/ml, P less than 0.05) and peak growth hormone responses after insulin were lower in the obese group (6.1 +/- 1.1 vs 12.7 +/- 3.7 ng/ml, P less than 0.05) than in controls. Whereas all control subjects had prolactin responses to both tests, five of 12 obese patients had no responses to insulin. Obese patients had lower prolactin responses at 30 minutes after insulin (5.4 +/- 0.7 vs 12.9 +/- 3.7 ng/ml, P less than 0.05) and lower prolactin responses at 60 minutes after TRH (9.9 +/- 1.7 vs 20.4 +/- 5.9 ng/ml, P less than 0.05). Maximum prolactin responses after TRH were lower in obese patients (9.9 +/- 2.0 vs 28.8 +/- 10.9 ng/ml, P less than 0.05). Maximum prolactin responses after insulin were lower in obese patients (6.2 +/- 4.1 vs 28.9 +/- 18.3 ng/ml). Thus prolactin secretion in childhood obesity is decreased after both stimuli, but more so after IV insulin that TRH, and suggests that, as in adult hypothalamic obesity, neuroendocrine regulation of prolactin release in obese children is impaired.

Adolescent↗
PubMed1979

Specific binding of prolactin by the prostate gland of the rat and man.

Specific binding sites for 125iodine-prolactin are present in membrane particles obtained from the rat ventral prostate, human benign prostatic hyperplasia and prostatic adenocarcinoma. In the ventral prostate glands of young rats (1 to 4 months old) specific binding of 125iodine-prolactin is higher than in older animals (greater than 8 months old). Subcellular distribution studies revealed that specific 125iodine-prolactin binding activity is associated primarily with the 15,000 and 100,000 g particulate membrane fractions of the rat ventral prostate and human prostate glands. In rats between 2 and 4 months old significant increases in the prolactin binding activity in the 100,000 g membrane fraction of the ventral prostate are observed to occur without concomitant increases in prolactin binding activity in the 15,000 g fraction. The level of specific 125iodine-prolactin binding activity present in the human prostate gland is lower than that observed in the rat ventral prostate gland. Localization of specific prolactin binding sites in the rat ventral psotate and the human prostate gland suggests that prolactin could influence the function of these tissues directly.

Animals↗
PubMed1975

Prostaglandin F2alpha (PGF2alpha) and prolactin secretion in rats.

Plasma prolactin and F-prostaglandins (PGF) were measured anesthetized male Sprague-Dawley rats before and at 15, 30, 45 and 60 minutes following i.v. injection of either PGF2alpha (4 mg/kg), chlorpromazine, 1 mg/kg or chlorpormazine (1 mg/kg) after pretreatment with i.p. indomethacin (2 mg/kg). Following PGF2alpha administration, plasma prolactin levels increased significantly only at 15 and 30 minutes in spite of extremely high PGF levels throughout 60 minutes. Besides the expected rise in plasma prolactin, chlorpromazine caused a transient but statistically significant increase in PGF. Indomethacin blocked the chlorpormazine-induced PGF rise but not prolactin increase. Animals stressed with ether anesthesia showed elevation of plasma prolactin, which was not blocked by indomethacin although PGF concentration fell. Theese results indicate that PGF2alpha can stimulate prolactin release. This effect does not appear to be physiologic since very high PGF levels are required. Furthermore, blockade of prostaglandin synthesis by indomethacin does not prevent the release of prolactin in response to chlorpormazine or stress. Our findings do not support a possible role of PGFs as intermediaries in prolactin release. However, it is possible that PGFs may work through other mechanisms not investigated in our study.

Animals↗
PubMed1982

Prolactin and estradiol increase striatal dopamine receptor density in intact, castrated and hypophysectomized rats.

1. Ovariectomized female or intact male rats were implanted with three adenohypophyses under the kidney capsule or treated with 17 beta-estradiol (10 micrograms twice daily) for 2 weeks. 2. In animals of both sexes, the pituitary-implanted and estradiol-treated rats had elevated plasma prolactin levels and had increased levels of striatal dopamine receptors. 3. We next investigated the possibility of an indirect action of estradiol via prolactin using hypophysectomized female rats (hypox) treated with 17 beta-estradiol or ovine prolactin (500 micrograms, twice daily) for 5 days. 4. Striatal dopamine receptor concentration was lower in hypox animals as compared to ovariectomized (85%, p less than 0.05) or intact female rats at random stage of the estrous cycle (76%, p less than 0.05) while the affinity (KD) of [3H]spiperone for these dopaminergic sites remained unchanged. 5. Treatment with estradiol or prolactin increased the level of striatal dopamine receptors (HYPOX + estradiol: 144% vs HYPOX, p less than 0.05; HYPOX + prolactin: 147% vs HYPOX, p less than 0.05). 6. These results indicate that high prolactin levels induced by pituitary implants or by injections of ovine prolactin lead, as observed with chronic estradiol treatment, to an increased density of striatal dopamine receptors. However, the effect of estradiol may not be explained exclusively by increased prolactin levels since the supersensitivity is also observed in hypophysectomized animals.

Animals↗
PubMed2000

Protein kinase C alpha, epsilon and AP-1 mediate prolactin regulation of mitochondrial aspartate aminotransferase expression in the rat lateral prostate.

Citrate accumulation and secretion are physiological functions of the prostate gland that are regulated by testosterone and prolactin. The metabolic pathway for citrate production in the prostate involves the activity of mitochondrial aspartate aminotransferase (mAAT). The expression of mAAT in the prostate is regulated by prolactin through a signal transduction pathway mediated by protein kinase C (PKC). In this report we determined which PKC isoforms are expressed in rat lateral prostate epithelial cells and their activation by prolactin. Eight PKC isoforms are expressed in the ventral and lateral prostate lobes. Although all eight isoforms are expressed, only PKCalpha and PKCvarepsilon were stimulated by prolactin and only in the lateral prostate lobe. Activator protein-1 (AP-1) appears to be the target of prolactin-PKC signaling because prolactin stimulated nuclear protein binding to an AP-1 consensus oligodeoxynucleotide. Moreover, the nuclear binding protein stimulated by prolactin also bound an mAAT oligodeoxynucleotide that contained an AP-1 consensus sequence and which competed for binding with the consensus AP-1 oligodeoxynucleotide. A PKCvarepsilon antisense oligodeoxynucleotide blocked expression of mAAT mRNA. Thus, we conclude that PKCvarepsilon is a specific PKC isoform that mediates via AP-1 the signal for prolactin regulation of mAAT gene expression in rat lateral prostate epithelial cells.

Animals↗
PubMed1999

The EGF response element in the prolactin promoter.

Epidermal growth factor (EGF) increases prolactin gene expression in GH4 cells, but the promoter element(s) required for this response has not been clearly defined. We identified a bipartite element - 96/ - 87, - 76/ - 67 in the rat proximal promoter that is essential for EGF signaling using deletion and linker-scanning mutants of the prolactin promoter. This element was active in either normal or inverted orientation when transferred to a heterologous promoter (mammary-tumor virus). We had previously identified this element as the cAMP/insulin response element of the prolactin promoter. However, the effects of EGF are additive with the responses to insulin or cAMP implying that EGF activated prolactin gene transcription by a mechanism different from insulin or cAMP. The EGF response element of the prolactin promoter is a recognition sequence for the Ets-related family of transcription factors and Ets-related factors have been shown to bind this element. Expression of the DNA-binding domain of c-Ets-1, which acts as a dominant negative inhibitor of Ets-related transcription factors, reduces EGF-increased prolactin-CAT expression 65% in GH4 cells. Thus, both EGF and insulin may signal through Ets-related transcription factors to activate prolactin gene transcription at the same response element in the prolactin proximal promoter.

Animals↗
PubMed2000

Nocturnal variation of prolactin secretion in the Mouflon (Ovis gmelini musimon) and domestic sheep (Ovis aries): seasonal changes.

Seasonal changes in nocturnal prolactin secretion and their relationship with melatonin secretion were monitored in wild (Mouflon, Ovis gmelini musimon) and domesticated sheep (breed Manchega, Ovis aries). Two groups of eleven adult females each, were maintained outdoors under natural photoperiod. Plasma concentrations of prolactin and melatonin were determined during the summer and winter solstices and the autumn and spring equinoxes. Blood samples were collected every 3h during the night hours, and 1h before and after the onset of darkness and sunrise. Maximum mean plasma concentrations of prolactin during the dark-phase in Mouflons were observed in the summer solstice, (P<0.001) and in the summer solstice and spring equinox in Manchega ewes (P<0.001). Mean plasma concentrations of prolactin were higher in the wild species (P<0.001) during the summer solstice. In contrast, during the spring equinox, mean levels of prolactin were higher in Manchega ewes than in Mouflons (P<0.05). Plasma prolactin concentrations showed a nocturnal rhythm in both breeds, with seasonal variations (P<0.001). The increase in plasma melatonin levels during the first hour after sunset was accompanied to increasing concentrations of PRL 1h after the onset of darkness, only in the autumn and spring equinox for the Mouflon, and in the summer solstice and spring equinox for the Manchega ewes. In Mouflons, the fall of plasma PRL concentrations about the middle dark-phase in all the periods studied, coincided with high levels of melatonin. A similar relation was observed in Manchega ewes only in the winter solstice and spring equinox. The current study shows that the nocturnal rhythm of prolactin secretion exhibits seasonal variation; differences in the patterns of prolactin secretion between Mouflon and Manchega sheep are taken to represent the effects of genotype.

Analysis of Variance↗
PubMed1998

Control of luteinizing hormone and prolactin secretion in birds.

In birds, the secretion of luteinizing hormone (LH) and prolactin is controlled by the releasing hormones, gonadotrophin releasing hormone-I (GnRH-I) and vasoactive intestinal polypeptide (VIP), respectively. The secretion of LH is depressed and the secretion of prolactin is at its highest, during incubation/brooding young and during the development of reproductive photorefractoriness. In incubating domestic chickens, decreased LH and increased prolactin secretion are correlated with decreased hypothalamic GnRH-I mRNA and increased hypothalamic VIP mRNA. Increased plasma prolactin contributes to the suppression of LH secretion in incubating poultry, possibly acting at the levels of the hypothalamus and the anterior pituitary gland. During the development of photorefractoriness, decreased plasma LH and increased plasma prolactin are correlated with decreased hypothalamic GnRH-I and increased hypothalamic VIP. In birds exposed to seasonal changes in daylength, the seasonally maximal concentrations of plasma prolactin associated with the development of photorefractoriness can be explained, in part, by the saturation daylength for photoinduced prolactin release being reached in late spring/mid summer. During the development of photorefractoriness, high concentrations of plasma prolactin play a role in ensuring the rapid regression of the gonads but are not essential for the maintenance of the condition.

Animals↗
PubMed2001

Prolactin response to dl-fenfluramine challenge before and after treatment with paroxetine.

The prolactin response to dl-fenfluramine (an indirect central serotonin agonist) challenge has been used to assess serotonergic function and appears to be blunted in depressed patients. We used this method to determine whether the serotonergic deficit in depressed patients is corrected by treatment with paroxetine. Prior to treatment with paroxetine sixteen depressed patients received a placebo challenge followed by a dl-fenfluramine challenge the next day. The same two challenges were repeated after treatment. Prolactin baseline levels were measured before pill administration, and then hourly for 5 hours. Fenfluramine/norfenfluramine levels were assayed at each time point after drug administration. Treatment with paroxetine significantly increased the baseline prolactin level independently of treatment response but positively correlated with paroxetine dose. We found that pre-treatment prolactin response to dl-fenfluramine challenge did not predict clinical response to paroxetine, nor did the prolactin response change significantly after treatment. There was no significant difference in the post-treatment prolactin response between treatment responders and treatment non-responders. We found evidence of increased prolactin levels that may reflect effects of paroxetine in enhancing serotonin levels. Acute release of serotonin as measured by the prolactin response to fenfluramine is not altered by paroxetine treatment.

Aged↗
PubMed1999

Prolactin and antipsychotic medications: mechanism of action.

Until the introduction of the first atypical antipsychotic, clozapine, in 1975, hyperprolactinemia was assumed to be an inevitable consequence of treatment with any antipsychotic agent. Now we know that atypical antipsychotics such as clozapine, olanzapine, quetiapine, sertindole, and ziprasidone are not associated with significant prolactin increase. These new antipsychotics appear to spare dopamine blockade within the brain's tubero-infundibular tract, a dopamine pathway that also controls prolactin secretion. Since the release of prolactin is tonically inhibited by the hypothalamus, with dopamine acting as the prolactin release-inhibiting factor, any disruption of the connection between the hypothalamus and the pituitary gland is associated with hyperprolactinemia. Other factors that can increase prolactin secretion are also reviewed (e.g. estrogens, thyroid-releasing factor, vasoactive intestinal peptides, opioids, surgery, illness such as epilepsy or herpes zoster infection, and psychic or physical stress). Prolactin levels are at their highest 1-2 hours before waking, and early waking interrupts its secretion. The major effects of hyperprolactinemia in women are amenorrhea, cessation of normal cyclic ovarian function, loss of libido, occasional hirsutism, and increased long-term risk of osteoporosis. The effects in men are impotence, loss of libido, and hypospermatogenesis. Current data indicate that conventional antipsychotics, as well as high doses of risperidone (> 6 mg/day), increase prolactin levels to a range associated with sexual dysfunction in nonpsychiatric patients. The lack of prolactin elevation reported with the atypical antipsychotics is believed to be due to their much greater specificity, which results in less blockade of dopamine receptors in the tubero-infundibular pathway.

Amenorrhea↗
PubMed2003

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

Prolactin, an anterior pituitary hormone, has been shown to have a role in immunomodulation. Some reports have shown the importance of prolactin in activating lymphocytes and macrophages, while in hyperprolactinemia patients, prolactin was found to decrease lymphocyte activation and natural killer function. In the present work, at physiological (15ng/ml) and stress-induced levels (30ng/ml) of prolactin, interferon-gamma (IFN-gamma) and interleukin (IL)-12 p70 levels, but not of IL-10 and tumor necrosis factor-alpha (TNF-alpha), increased significantly (p<0.05-0.006) in phytohemeagglutinin (PHA)+lipopolysaccharide (LPS)-stimulated whole blood. However, no such effect was observed at high concentrations of prolactin (100-300ng/ml). In addition, 15ng/ml of prolactin reversed hydrocortisone suppressive effect on IFN-gamma, IL-12 p70, and IL-10 production in PHA+LPS-stimulated whole blood. On the other hand, in LPS-stimulated whole blood, prolactin enhanced significantly (p=0.027) the production levels of IL-10, but not of IFN-gamma, IL-12 p70, and TNF-alpha, in non-concentration-dependent manner. These results suggest that prolactin modulates cytokine response during antigenic response, and this modulation is stimulus specific.

Adult↗