Central IL-1 differentially regulates peripheral IL-6 and TNF synthesis

Kitamura, Hiroshi; Okamoto, Susumu; Shimamoto, Yoshinori; Morimatsu, Masami; Terao, Akira; Saito, Masayuki

doi:10.1007/s000180050151

Cited by 18 publications

(9 citation statements)

References 30 publications

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“…In contrast, chlorisondamine (0.5 mg/kg) did not block epibatidine stimulation of the hypothalamic-pituitary-adrenal axis (Mellon and Bayer, 1999), which is mediated by central nicotinic receptor stimulation (Matta et al, 1987). Consistent with a role of the autonomic ganglia to elevate IL-6, pretreatment of animals with chlorisondamine (3 mg/kg) also prevented IL-1␤-stimulated sera IL-6 levels (Kitamura et al, 1998). Therefore, these data provide the first evidence that stimulation of peripheral ganglionic nicotinic receptors was required for the elevation of plasma IL-6 by morphine.…”

Section: Downloaded Fromsupporting

confidence: 74%

Rapid Elevation of Plasma Interleukin-6 by Morphine Is Dependent on Autonomic Stimulation of Adrenal Gland

Houghtling

Bayer²

2002

J Pharmacol Exp Ther

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Several studies have demonstrated that opioids regulate a number of immune cell functions either through direct mechanisms or through the modulation of central nervous system outputs. It has been previously shown that morphine increases serum interleukin-6 (IL-6) levels; however, the mechanism by which this effect is produced is unknown. In the present study, experiments were designed to address the potential role of central opioid receptors, peripheral autonomic ganglia, and activation of the adrenals in the elevation of plasma IL-6 after morphine administration. A rapid and significant (2-fold) increase in plasma IL-6 was observed after morphine administration (10 mg/kg s.c.) to rats. This effect of morphine peaked within 30 min and remained elevated for at least 2 h. Central microinjection of morphine (10 g/2 l i.c.v.) mimicked the effects of peripherally administered morphine and was completely blocked by naltrexone (10 mg/kg s.c.) pretreatment. Pretreatment with a ganglionic blocker, chlorisondamine (0.5 mg/kg i.p.), also blocked the elevation of IL-6 by morphine, suggesting a role of the autonomic nervous system. In adrenalectomized animals, morphine administration did not increase IL-6 levels, whereas in adrenal demedullated animals, the effect of morphine remained intact. Thus, the adrenal cortex may be a potential source of IL-6, because IL-6 mRNA has been localized in the adrenal gland. Collectively, these data suggest a unique mechanism by which stimulation of central opioid receptors results in the elevation of plasma IL-6 through autonomic activation specifically of the adrenal cortex.

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Section: Downloaded Fromsupporting

confidence: 74%

Rapid Elevation of Plasma Interleukin-6 by Morphine Is Dependent on Autonomic Stimulation of Adrenal Gland

Houghtling

Bayer²

2002

J Pharmacol Exp Ther

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“…Although, NF‐κB is generally viewed as an anti‐apoptotic and pro‐inflammatory factor, recent evidence suggest that NF‐κB may promote apoptosis during tumour progression (Radhakrishnam and Kamalakaran, 2006; Perkins, 2004), and may also have an anti‐inflammatory roles (Lawrence and Fong, 2010). We suggest that NF‐κB might mediate cell‐growth inhibition by up‐regulation of its target genes, such as IL‐6 expression, which has an inhibitory effect on the growth of LNCaP cells (Kitamura et al, 1998; Stratton‐Maliner et al, 2001; Hobisch et al, 2001; Spiotto and Chung, 2000). NF‐κB also mediates pro‐apoptosis in LNCaP by a TRADD (tumour‐necrosis‐factor‐associated death domain)‐dependent repression of AR promoter through TNFα stimulation (Wang et al, 2009).…”

Section: Discussionmentioning

confidence: 96%

Involvement of interleukin‐1β mediated nuclear factor κB signalling pathways to down‐regulate prostate‐specific antigen and cell proliferation in LNCaP prostate cancer cells

Bouraoui

Raïs

Čulig

et al. 2012

Cell Biology International

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Involvement of NF-κB (nuclear factor κB) mediated by IL-1β (interleukin-1β) on cell proliferation and PSA (prostate-specific antigen) production of LNCaP prostate cell lines and the possible cross-talk with Akt (also known as protein kinase B) signalling pathway has been investigated. NF-κB and Akt were analysed by Western blotting from LNCaP cells treated by IL-1β before proliferation and PSA production were measured. IL-1β inhibited proliferation and decreased PSA production. The Akt pathway was not sensitive, whereas NF-κB phosphorylation occurred as a result of treatment. PSA production and proliferation of LNCaP cells were down-regulated by NF-κB mediated by IL-1β promoting anti-apoptotic signalling and co-suppressor factors of PSA expression. IL-1β through NF-κB activation provides a rationale for therapeutic approaches in the anticancer treatment of prostate.

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“…IL-6 was not secreted by either untreated cells or those treated with TNF . a or IL-1 b, known to act as inducers of expression of the IL-6 gene (data not shown; Kohase et al 1986, Kitamura et al 1998.…”

Section: Expression Of Il-6 and Il-6r In Lapc-4 And Mda Pca 2b Cellsmentioning

confidence: 94%

Interleukin-6 stimulation of growth of prostate cancer in vitro and in vivo through activation of the androgen receptor

Malinowska¹,

Neuwirt²,

Cavarretta³

et al. 2009

Endocrine-Related Cancer

145

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It is hypothesized that ligand-independent activation of the androgen receptor is one of the mechanisms implicated in tumour progression. However, supportive evidence is limited to the effect of HER-2/neu that stimulates prostate cancer progression through activation of the androgen receptor. In the present study, we have asked whether the proinflammatory cytokine interleukin-6 (IL-6), which is known to stimulate androgen receptor activity and expression of its downstream target genes, may also induce growth of androgen-sensitive cells. We have found that IL-6 differentially regulates proliferation of LAPC-4 and MDA PCa 2b cells. In MDA PCa 2b cells, growth stimulation by IL-6 was reversed by administration of either the non-steroidal anti-androgen bicalutamide or the inhibitor of the mitogen-activated protein kinase pathway PD98059. Neither cell line was found to express endogenous IL-6. Interestingly, the treatment of those prostate cancer cells did not increase phosphorylation of STAT3. The effect of IL-6 on stimulation of androgen receptor activity in MDA PCa 2b cells was lower than that of androgen, comparable with findings reported by other researchers. However, growth of MDA PCa 2b xenografts in castrated animals treated with IL-6 was similar to that in non-castrated animals. In addition, bicalutamide showed an inhibitory effect on IL-6-regulated growth in vivo. Taken together, data in the present study demonstrate that IL-6 may cause growth of androgen receptorpositive tumours in vitro and in vivo through activation of the androgen receptor.

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Central IL-1 differentially regulates peripheral IL-6 and TNF synthesis

Cited by 18 publications

References 30 publications

Rapid Elevation of Plasma Interleukin-6 by Morphine Is Dependent on Autonomic Stimulation of Adrenal Gland

Rapid Elevation of Plasma Interleukin-6 by Morphine Is Dependent on Autonomic Stimulation of Adrenal Gland

Involvement of interleukin‐1β mediated nuclear factor κB signalling pathways to down‐regulate prostate‐specific antigen and cell proliferation in LNCaP prostate cancer cells

Interleukin-6 stimulation of growth of prostate cancer in vitro and in vivo through activation of the androgen receptor

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