Reduced natural killer (NK) activity in patholoical hyperprolactinaemia

Gerli, Roberto; Migliorati, Graziella; Nicoletti, Ildo; Rambotti, P; Riccardi, C

doi:10.1016/0192-0561(85)90241-3

Cited by 8 publications

(11 citation statements)

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“…Moreover, PRL has the ability to exert immunostimulatory or immunosuppressive effects, depending on its level and the pathophysiological conditions (17). For example, physiological concentrations of PRL (<0.02 μg/ml) are more effective than high PRL levels (0.1 μg/ml) in stimulating antibody production by SLE lymphocytes (64), low PRL levels stimulate and high levels inhibit NK cell proliferation (65), and hyperprolactinemic patients (mean serum PRL of 0.98 μg/ml or 0.20 μg/ml) show reduced NK cell numbers (66) and function (67). Also, hyperprolactinemia protects against inflammatory arthritis in rats (present study), and treatment with a high, but not a low, dose of PRL exacerbates experimental MS (61).…”

Section: Discussionmentioning

confidence: 99%

Prolactin promotes cartilage survival and attenuates inflammation in inflammatory arthritis

et al. 2013

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Chondrocytes are the only cells in cartilage, and their death by apoptosis contributes to cartilage loss in inflammatory joint diseases, such as rheumatoid arthritis (RA). A putative therapeutic intervention for RA is the inhibition of apoptosis-mediated cartilage degradation. The hormone prolactin (PRL) frequently increases in the circulation of patients with RA, but the role of hyperprolactinemia in disease activity is unclear. Here, we demonstrate that PRL inhibits the apoptosis of cultured chondrocytes in response to a mixture of proinflammatory cytokines (TNF-α, IL-1β, and IFN-γ) by preventing the induction of p53 and decreasing the BAX/BCL-2 ratio through a NO-independent, JAK2/STAT3-dependent pathway. Local treatment with PRL or increasing PRL circulating levels also prevented chondrocyte apoptosis evoked by injecting cytokines into the knee joints of rats, whereas the proapoptotic effect of cytokines was enhanced in PRL receptor-null (Prlr -/-) mice. Moreover, eliciting hyperprolactinemia in rats before or after inducing the adjuvant model of inflammatory arthritis reduced chondrocyte apoptosis, proinflammatory cytokine expression, pannus formation, bone erosion, joint swelling, and pain. These results reveal the protective effect of PRL against inflammation-induced chondrocyte apoptosis and the therapeutic potential of hyperprolactinemia to reduce permanent joint damage and inflammation in RA.

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Section: Discussionmentioning

confidence: 99%

Prolactin promotes cartilage survival and attenuates inflammation in inflammatory arthritis

et al. 2013

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“…15 The immunosuppressant effect of increased levels of prolactin may be due in part to a decreased natural killer cell activity in the presence of hyperprolactinemia. 14,16 Another explanation for the fewer relapses experienced by breast-feeding compared to non-breast-feeding mothers may be the immune suppression resulting Breast-feeding compared to non-breast-feeding mothers had statistically significantly fewer relapses during the zero-to three-month period.…”

Section: Ms Relapses On Elimination Symptomsmentioning

confidence: 99%

Influence of Infant Feeding Method on Postpartum Relapse of Mothers With MS

Gulick

Halper

2002

International Journal of MS Care

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In an effort to determine relapse rates in breast-feeding and non-breast-feeding mothers with multiple sclerosis (MS) as well as differences in symptom prevalence between relapsing and non-relapsing mothers following delivery among breast-feeding mothers compared with non-breast-feeding mothers have implications for encouraging women with MS who wish to breast-feed their infants to do so, particularly if their pregnancy was free of relapse. Women with MS are also encouraged to postpone the initiation of immunomodulating therapy until three months following delivery or when breast-feeding is discontinued. (Int J MS Care. 2002;4:183-191) F ew studies have been conducted regarding the effects of breast-feeding on relapse rates during the postpartum period among women with multiple sclerosis (MS), and those that have been conducted report dissimilar findings. Retrospective studies report relapse rates between .375 and .440 for breast-feeding and .305 and 1.00 for non-breast-feeding mothers during the first nine and 12 months postpartum.1,2 In a prospective study consisting of four breast-feeding and four non-breast-feeding mothers, Birk et al 3 reported annualized relapse rates of 3.0 and 1.74 for the threeand six-month postpartum periods, respectively. Another prospective study reported relapse rates of 1.2 at three months and .9 at six months postpartum for breast-feeding mothers compared with 1.30 and 1.0 respectively for non-breast-feeding mothers.4 These studies varied in sample size and, with the exception of one study, 4 failed to control for potential confounding factors that may influence relapse rates.Unless potentially confounding influences on relapse rates are controlled, the true effects of breast-feeding on relapse rates cannot be discerned. The purpose of the Elsie E.

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“…The lymphocytes of elderly healthy donors (Nagel et al, 1988;Orson et al, 1989) and cancer patients (Pross and Baines, 1986;Roszman et al, 1991) are known to be deficient in Interleukin-2 (IL-2) secretion and IL-2 receptor (IL-2R) expression, which may be the major contributory factors in development of immunodeficiency. Involvement of the pituitary peptide hormone prolactin (Prl) in immunoregulation is suggested by the hormone-mediated control of lymphoid cell growth and function (Bernton 1989;Berczi et al, 1991;Hooghe et al, 1993), reversal of glucocorticoid (GC)-mediated immunosuppression (Biswas and Chattopadhyay, 1992), improved functioning of the depressed immune system in the aged (Homo-Delarche and Durant, 1994) and impaired immune functions in hyperprolactinemic patients (Gerli et al, 1986). Prl-induced immunomodulation is mediated by the Prl receptors (Prl-R) present on the cell surface of various leukocytes (Russell er al., 1985).…”

Section: Prolactin Response Of Nk Cells But Not Of Lak Cells Is Defmentioning

confidence: 99%

Prolactin response of NK cells, but not of LAK cells, is deficient in patients with carcinoma of oral cavity and during aging

Chakraborty

Chattopadhyay

1996

Int. J. Cancer

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The regulatory role of prolactin (Prl) on peripheral blood natural killer (NK) and lymphokine-activated killer (LAK) cell activities was studied in young (mean age, 40 years) and elderly (mean age, 68 years) healthy men and patients with carcinoma of the oral cavity (oral cancer). The peripheral blood NK cells, but not the LAK cells, were found to be depressed in oral cancer patients compared with age-matched healthy men. However, age-associated deficiency in both NK and LAK cell activity was observed in healthy men and cancer patients. Prl produced dosedependent inhibition (I, 10, 100 or 250 ng/ml) or stimulation (25-50 ng/ml) of resting NK cells in young groups of healthy men and cancer patients. In elderly groups less or no response of the NK cells to low doses of Prl (I-I 0 ng/ml) was evident. The NK cells of young and elderly healthy men were stimulated by human recombinant Interleukin-2 (rlL-2) (100 U/ml), and Prl (1-250 ng/ml) inhibited these cells. In oral cancer patients an altered response to low doses of Prl(1-50 ng/ml) was observed in IL-2-stimulated NK cells, which also revealed malignancyassociated loss of IL-2 response. In contrast, there was no malignancy or age-associated change in Prl response of the LAK cells. Treatment of peripheral blood lymphocytes of both healthy men and oral cancer patients for 5 days with Prl(50 ng/ml) in the presence of low concentration of serum generated LAK cells.o 1996 Wiley-Liss, Inc.

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Reduced natural killer (NK) activity in patholoical hyperprolactinaemia

Cited by 8 publications

References 0 publications

Prolactin promotes cartilage survival and attenuates inflammation in inflammatory arthritis

Prolactin promotes cartilage survival and attenuates inflammation in inflammatory arthritis

Influence of Infant Feeding Method on Postpartum Relapse of Mothers With MS

Prolactin response of NK cells, but not of LAK cells, is deficient in patients with carcinoma of oral cavity and during aging

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