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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effect of interleukin-6 (IL-6) on second messenger systems in anterior pituitary (AP) cells. The acute exposition of membranes derived from the pituitary gland to IL-6 did not modify basal and forskolin-stimulated adenylate cyclase (AC) activity, as well as inositol phosphate (IP) production and free [Ca(++)]i. Preincubation of AP cells with IL-6 for 20 min did not affect basal second messengers levels, while completely abolished the stimulation by VIP of AC activity, partially inhibited forskolin-stimulated cAMP formation and reduced TRH-stimulated IP production. Finally, the pretreatment of AP cells for 20 min with IL-6 also reduced the TRH-induced rise in free [Ca(++)]i.
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PMID:Interleukin 6 modulation of second messenger systems in anterior pituitary cells. 140 45

Interleukin-6 (IL-6) is a pleiotropic cytokine exerting many immunological and non immunological actions. The cytokine binds to a specific receptor, whose activation induces the association with a novel transducer, the glycoprotein gp 130. Here we present our results about the effect of IL-6 on both hormone secretion and second messenger systems at pituitary level, and the production of IL-6 from cells of central nervous system. IL-6 inhibited basal, VIP and TRH-stimulated prolactin (PRL) secretion from single lactotropes, studied by means of reverse hemolytic plaque assay, whereas in primary cultures of anterior pituitary cells, according to the literature, the cytokine stimulated prolactin secretion. IL-6 did not affect basal adenylate cyclase activity, inositol phosphate production, and cytosolic calcium concentration. Conversely, the preincubation of pituitary cells with interleukin-6 for 20 min significantly reduced VIP- and forskolin-stimulated adenylate cyclase activity, as well as inositol phosphate production and free cytosolic calcium increase induced by TRH.
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PMID:Role of interleukin-6 in the neuroendocrine system. 166 73

Interleukin-6 (IL-6), a cytokine produced by inflammatory reactions, was found to stimulate PRL, GH and LH release from anterior pituitary cells at concentrations similar to those which affected lymphocyte mitogenesis. Perifused pituitary cells responded to IL-6 with prompt increases in hormone release that declined rapidly following cessation of exposure. Dopamine (DA) attenuated IL6-induced PRL release. In addition, IL-6 potentiated both GHRF- and TRH-induced hormone release without an affect on intracellular cAMP. These data demonstrate a new biological activity for IL-6 and provide evidence for immune system regulation of anterior pituitary hormone release.
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PMID:Interleukin-6 stimulates anterior pituitary hormone release in vitro. 254 14

The synovial fluid of patients with rheumatoid arthritis (RA) contains a biologically active factor which has the ability to replace T cells for the induction of antibody secretion by human blood lymphoid cells stimulated by pokeweed mitogen (PWM) in vitro. This factor, which will be referred to as RA-SF (synovial fluid), also has the capacity to act as a B cell-stimulatory factor of mouse splenic lymphocytes in the presence of lipopolysaccharide (LPS). Using a test system developed for the definition of interleukin 4 (IL-4), which is a B cell-stimulating lymphokine which preferentially activates the synthesis of selected Ig classes in mouse lymphoid cells, we have shown that RA-SF has properties similar to IL-4 in that it induces differentiation of antibody secretion in the LPS-pretreated mouse cell, but unlike IL-4, which gives IgG1 and IgE, it selectively induces IgG2b synthesis. The present study demonstrates that RA-SF has a biological activity that is reminiscent of other B cell-stimulating mouse lymphokines, but it is biologically distinct from IL-2, IL-4, and IL-5. Recent data also indicate that it is distinct from gamma interferon (IFN-gamma). Therefore, we conclude that the biological activity of RA-SF has properties in common with a T-cell replacing (TRF) and B-cell differentiation factor (BCDF) and probably represents yet another biological activity which so far lacks an experimental counterpart. The relevance of this factor for autoantibody synthesis is discussed.
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PMID:Biological characterization of T cell-replacing factor in the synovial fluid of rheumatoid arthritis patients. 326 Jun 84

Recent evidence has revealed that various neuropeptides appear to have distinct roles as immunomodulators. The aim of this study was to evaluate the role of hypothalamic neuropeptides (thyreoliberin [TRH], somatostatin [SRIF], and gonadoliberin [LH-RH]) on the secretion of interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) from lipopolysaccharide (LPS) activated human peripheral blood monocytes (PM) cultured in vitro. LPS in concentration 1.5 micrograms/ml stimulated PBM to release IL-1 beta or IL-6 into the supernatants. SRIF in concentrations from 10(-8)M to 10(-10)M (but neither RH nor LH-RH in the same concentrations) potentiated the release of IL-6 from PBM. None of the tested neuropeptides stimulated the release of IL-1 beta from LPS activated human monocytes. These data indicate that SRIF in physiological or pharmacological concentrations which activate the release of IL-6 from PBM may be one of the regulators of immune response in humans.
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PMID:Somatostatin (SRIF) stimulates the release of interleukin-6 (IL-6) from human peripheral blood monocytes (PBM) in vitro. 747 64

We analyzed serum levels of interleukin-6 (IL-6) and seven acute phase proteins in CRP positive samples and in patients with open heart surgery. The concentrations of serum IL-6 were not correlated with other acute phase proteins in CRP positive samples. However, IL-6 were in inverse correlation with CRP, AAG, AAT and CER in patients with open heart surgery. These discrepancies were due to the differences in response time of each acute phase protein after the start of inflammation. Responses of acute phase proteins after open heart surgery were investigated from hour to hour. IL-6 increased rather rapidly than other acute phase proteins, and increases of CRP, TRF, AAT, AAG, CER, HAP and AMG followed. The time reached the peak were IL-6, CRP, TRF, AAT, AMG, AAG, HAP reached the peak in that order. IL-6 constantly increased seven hours earlier, and reached at maximum values forty three hours earlier than CRP in each case. The measurement of serum concentration of IL-6 may be useful for early detection of acute inflammation.
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PMID:[The clinical significance of interleukin-6 as an inflammatory marker (the studies in patients with open heart surgery)]. 753 Dec 52

Since serum concentrations of tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and interleukin-6 (IL-6) are elevated in infectious and inflammatory illnesses, we examined their potential role in contributing to the low TSH concentrations associated with such conditions, both at the level of the pituitary and the hypothalamus. 20 hours exposure to recombinant murine TNF-alpha (10(-11) to 10(-10) mol/l) enhanced the basal and the TRH-stimulated release of TSH by cultured rat anterior pituitary cells, but 4 hours exposure increased only basal TSH secretion. Recombinant human (rh) IL-1 beta, at a dose of 10(-11) mol/l only, produced a very small increase in basal TSH secretion after 4h, but not 20h, exposure. TRH-stimulated TSH secretion was not affected by IL-1 beta in concentrations up to 10(-10) mol/l, at either exposure time. Rh IL-6 (10(-12) to 10(-9) mol/l), had no effect on basal or TRH-stimulated TSH secretion at either exposure time. TNF-alpha, IL-1 beta, and IL-6 all failed to modify the inhibitory response to triiodothyronine (T3) and thyroxine (T4) on TSH secretion, under basal or TRH-stimulated conditions. Indirect effects of the cytokines on the stimulation or inhibition of TSH secretion, via TRH or SRIF respectively, were tested in isolated rat hypothalamic slices. 30 min exposure to TNF-alpha, IL-1 beta, or IL-6 had no effect on the basal release of SRIF. However, IL-1 beta, from 2.5 x 10(-12) to 10(-10) mol/l, produced a dose-dependent enhancement of the SRIF released by 5 x 10(-2) mol/l extracellular K+. The effect appeared to be mediated via IL-1 receptors, and to involve prostanoid formation, since it was inhibited by IL-1 receptor antagonist protein, 10(-7) mol/l, and indomethacin, 2.8 x 10(-5) mol/l, respectively. Neither basal nor K(+)-stimulated TRH release was influenced by TNF-alpha, IL-1 beta, or IL-6. The results indicate that direct effects of these cytokines on the pituitary do not contribute to reduced circulating TSH concentrations during inflammation and infection, but that enhanced hypothalamic release of SRIF, in response to elevated IL-1 beta, could contribute to such a decrease in TSH. None of the cytokines tested decreased hypothalamic TRH release in vitro. However, further in vivo experiments would be required to determine whether a longer exposure to these agents could reduce TRH release either directly, or indirectly via inputs from outside the hypothalamus.
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PMID:Effect of interleukin-1 beta, tumour necrosis factor-alpha and interleukin-6 on the control of thyrotropin secretion. 762 15

Interleukin-2 (IL-2) is a pluripotential cytokine that, besides its role in the regulation of immunocompetent cells function, also stimulates hormone secretion. On the other hand, several factors, including cytokines (interleukin-1, IL-1; interleukin-6, IL-6) and pituitary hormones (thyrotropin, TSH; prolactin, PRL), exert stimulatory effects on T-cell connected IL-2 production. In order to evaluate the role of both pituitary hormones in the activation of the immune system, the following two standard diagnostic tests were performed: TRH test (0.2 mg) in 8 healthy human subjects (4F/4M) aged 18-50 years, and oral metoclopramide (MCP) test (10 mg) in 8 females with galactorrhea and regular menstruation aged 18-52 years. The mobilization (peak response) of PRL, TSH, triiodothyronine (T3), thyroxin (T4), IL-1 beta, IL-2, IL-6 in TRH test, and PRL, IL-1 beta, IL-2, IL-6 for MCP test were evaluated. The responses of TSH (2.0 +/- 0.3 vs 12.3 +/- 2.2 microlU/ml, p < 0.01), PRL (15.3 +/- 2.3 vs 46.4 +/- 8.8 ng/ml, p < 0.01), T3 (178.0 +/- 16.4 vs 248.7 +/- 21.1 ng/dl, p < 0.001), T4 (7.9 +/- 0.4 vs 9.6 +/- 0.5 micrograms/dl, p < 0.001), and IL-2 (45.6 +/- 7.8 vs 79.9 +/- 16.4 fmol/ml, p < 0.05) in TRH test were noted. The peak response of PRL (16.3 +2- 2.6 vs 107.7 +/- 22.4 ng/ml, p < 0.01) in MCP test was also observed, but without any changes in interleukin concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased interleukin-2 levels during standard TRH test in man. 781 86

By using an AtT20 cell line transfected with complementary DNA for preproTRH, we have identified the proTRH polyeptide precursor [26 kilodaltons (kDa)] and shown that this molecule gives rise to the proTRH derived sequences as determined by pulse-chase and trypsinization studies. The predicted proTRH precursor composed of 231 amino acids with 5 copies of a TRH progenitor sequence (Gln-His-Pro-Gly) and 7 other cryptic peptides was demonstrated by: 1) Western Blot analysis of an AtT20 cell extract with anti-pCC10 antibodies (an antibody that recognizes the intact prohormone as well as some intermediate products of processing); 2) Immunoprecipitation of the radiolabelled 26 kDa protein with anti-pCC10 followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis; 3) Gel filtration chromatography of the radiolabeled 26 kDa extracted from SDS-PAGE. 4) RIA with anti-pCC10 antiserum against peptides extracted from adult rat hypothalamus and olfactory lobe after SDS-PAGE. 5) Trypsinization of the proTRH precursor which generated the proTRH cryptic peptides preproTRH25-50 (pYE27) and preproTRH53-74 (pFT22). These moieties were also produced during trypsinization of intermediate products of processing. By means of pulse-chase studies, the 26 kDa polypeptide was shown to be the biosynthetic precursor to all the proTRH derived cryptic peptides. Cleavage at two positions in the center of the molecule (Lys107-Arg108 and Lys152-Arg153) generated two moieties of 16.5 and 15 kDa. The 15 kDa N-terminal fragment is later cleaved to a 6 kDa peptide that includes the proTRH derived peptides, pYE27, pFT22, and pEH24. The carboxy-terminal 16.5 kDa fragment of the prohormone is processed to a 9.6 kDa fragment which contains the proTRH derived peptide pST10 (preproTRH160-169) and a fragment of 5.4 kDa that may be the C-terminal peptide preproTRH208-255 recognized by antisera pAC12 and pYE17. In further processing, the 9.6 kDa molecule is cleaved to produce a 5.4 kDa peptide from either sequences 115-169 or 160-199.
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PMID:Identification of the thyrotropin-releasing hormone-prohormone and its posttranslational processing in a transfected AtT20 tumoral cell line. 844 Jan 87

Interleukins are proteins involved in the immune system and have been related to the endocrine regulation of the hypothalamic-pituitary-adrenal axis as well as to the secretion of ACTH, prolactin (PRL), GH and, possibly, LH. Like interleukin-6 (IL-6), vasoactive intestinal peptide (VIP) is synthesized in the pituitary gland and stimulates prolactin secretion. The aim of the present study was to address whether Interleukin 6 is involved in the regulation of VIP, as well as other factors involved in the regulation of prolactin such as dopamine, TRH and estradiol. Accordingly, we performed an in vitro study on monolayer cultures of rat pituitary cells, neutralizing the possible paracrine effect of IL-6 by immunosuppressing the protein by treatment with polyclonal antibody against IL-6 over 1, 3, 6 or 24 hours and then determining the degree of proliferation of VIP cells using double immunocytochemical labelling for VIP or PRL and proliferating cell nuclear antigen (PCNA). As a control, the effects of immunosuppression on the proliferation of PRL-positive cells were analyzed. Immunosuppression of IL-6 induced modifications in the cellular and nuclear size of VIP-positive cells, indicating an inhibitory process. Moreover, immunosuppression induced a significant decrease in the proliferation rate of PRL-positive or VIP-positive cells for all time-points analyzed. Similar effects on the proliferation rate of PRL-positive cells were found. The results of the present study demonstrate that IL-6 is involved in the regulation of the activity and proliferation of pituitary VIP-producing cells and suggest that, without ruling out a direct effect of IL-6 on prolactin cells, IL-6 could regulate prolactin by acting on pituitary VIP.
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PMID:The activity and proliferation of pituitary prolactin-positive cells and pituitary VIP-positive cells are regulated by interleukin 6. 2370 Feb 4


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