Growth hormone and prolactin expression in the immune system

Prolactin (PRL) and growth hormone (GH) are pituitary hormones that play pivotal roles in lactation and body growth, respectively. In addition, both hormones have been implicated as modulators of immune responses. Since the expression of GH and PRL by leukocytes points to autocrine or paracrine roles during immune responses, our study is aimed at PRL- and GH-production in leukocytes. We show that human peripheral blood granulocytes, which express GH and PRL mRNA, contain high molecular-weight immunoreactive variants of GH and PRL (37 and 43 kDa, respectively), but not the pituitary-sized hormones. Secretion of these variants, or biologically active material as assessed by the Nb2 bioassay, was not detected. On the other hand, certain leukemic myeloid cells secrete 23-kDa, pituitary-sized, PRL, which is biologically active

Effects of prolactin on cloned human T-Lymphocytes

To evaluate the possible role of prolactin (PRL) in T-lymphocytes, we monitored gene induction in one cytotoxic T-lymphocyte (CTL) clone derived from a patient with hemochromatosis and in several T-helper clones generated from a normal donor and a patient with multiple sclerosis. The CTL clone expressed conventional PRL receptor (PRLR), and PRL induced the expression of suppressor of cytokine signaling-3 (SOCS-3) and increased the expression of SOCS-2 and cytokine-inducible src homology-2-containing protein (CIS, another member of the SOCS family). As is the case in granulocytes, expression of a conventional receptor for PRL could not be shown by polymerase chain reaction analysis on three helper clones. In addition, as in granulocytes, PRL modulated the expression of genes such as the interferon-regulatory factor-1, inducible nitric oxide synthase, CIS, and SOCS-2. These effects were also elicited with ovine PRL and could be prevented by anti-PRL antibodies. Thus, the use of clones allowed the detection of direct effects of PRL on T-cells, even when these have few or no detectable MR, confirming that human T-lymphocytes are targets for PRL

Effects of prolactin on cloned human T-Lymphocytes

To evaluate the possible role of prolactin (PRL) in T-lymphocytes, we monitored gene induction in one cytotoxic T-lymphocyte (CTL) clone derived from a patient with hemochromatosis and in several T-helper clones generated from a normal donor and a patient with multiple sclerosis. The CTL clone expressed conventional PRL receptor (PRLR), and PRL induced the expression of suppressor of cytokine signaling-3 (SOCS-3) and increased the expression of SOCS-2 and cytokine-inducible src homology-2-containing protein (CIS, another member of the SOCS family). As is the case in granulocytes, expression of a conventional receptor for PRL could not be shown by polymerase chain reaction analysis on three helper clones. In addition, as in granulocytes, PRL modulated the expression of genes such as the interferon-regulatory factor-1, inducible nitric oxide synthase, CIS, and SOCS-2. These effects were also elicited with ovine PRL and could be prevented by anti-PRL antibodies. Thus, the use of clones allowed the detection of direct effects of PRL on T-cells, even when these have few or no detectable MR, confirming that human T-lymphocytes are targets for PRL

Regulation of prolactin expression in leukemic cell lines and peripheral blood mononuclear cells

To address the role of different intracellular signals in prolactin (PRL) expression in leukocytes, we have investigated the effects of chlorophenylthio-cAMP (cptcAMP), phorbol myristate acetate (PMA) and ionomycin on the activation of the upstream PRL promoter in several leukemic cell lines. All three stimulators, alone or in synergism with each other, were able to modulate promoter activity, but their actions were cell-type dependent. In freshly isolated peripheral blood mononuclear cells (PBMC), PRL expression could only be stimulated by cptcAMP. The physiological importance of cAMP in the regulation of PRL expression in leukocytes is suggested by the finding that in PBMC, PRL expression is enhanced by prostaglandin-E2 and the β2-adrenergic agonist terbutaline, which both signal through cAMP. © 2002 Elsevier Science B.V. All rights reserved.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Inhibition of cytokine production by the herbicide atrazine - Search for nuclear receptor targets

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Pituitary growth hormone release and gene expression in cafeteria-diet-induced obese rats

In human obesity as well as in rat obesity models a decrease in spontaneous and stimulated GH secretion has been a constant finding, The presence of a decreased pituitary GH synthesis in diet-induced obese male rats was investigated and its possible relationship with obesity-related changes in peripheral hormones was analyzed. Cafeteria-diet-overfed obese male Wistar rats with body fat percentage above 30% had a significantly decreased pituitary GH mRNA transcript level assessed by both Northern blot and in situ hybridization, and a lower pituitary GH protein level as demonstrated by immunocytochemistry. The GH transcript level con-elated negatively with the serum leptin and positively with the IGF-I concentration. No differences in circulating tri-iodothyronine, non-Easting insulin and corticosterone levels were found between overfed and control rats. GH release by cultured pituitary cells from overfed rats Tvas comparable to that by cells prepared from control rats. In contrast, incubation of normal pituitary cells with serum from overfed rats for 3 days gave a significantly lower GH release than after incubation with serum from non-obese rats. In conclusion, cafeteria-diet-induced obese male Wistar rats have a decreased pituitary GH gene expression and a modifiable GH release in in vitro experiments. A possible role for peripheral circulating factors, like leptin and IGF-I, in decreasing the pituitary GH synthesis and release in obese rats is discussed