VIP and PACAP inhibit IL-12 production in LPS-stimulated macrophages. Subsequent effect on IFNgamma synthesis by T cells.

Delgado M; Munoz Elias-EJ; Gomariz RP; Ganea D

首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >VIP and PACAP inhibit IL-12 production in LPS-stimulated macrophages. Subsequent effect on IFNgamma synthesis by T cells.

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VIP and PACAP inhibit IL-12 production in LPS-stimulated macrophages. Subsequent effect on IFNgamma synthesis by T cells.

机译：VIP和PACAP抑制LPS刺激的巨噬细胞中IL-12的产生。 T细胞对IFNγ合成的后续影响。

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Since IL-12 plays a central role against intracellular pathogens, and contributes to the pathogenesis of immune diseases, its regulation is essential. This study examines the effect of two neuropeptides, vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase activating polypeptide (PACAP), on interleukin-12 (IL-12) production. VIP/PACAP inhibit IL-12 dose-dependently. Type 1 VIP receptor (VPAC1), and to a lesser degree type 2 VIP receptor (VPAC2), mediate the inhibition of IL-12, primarily through the cAMP/PKA pathway. VIP/PACAP inhibit the production of IL-12, IL-6, tumor necrosis factor alpha (TNFalpha), and interferon gamma (IFNgamma) in vivo in endotoxemic mice. The presence of VIP/PACAP in the lymphoid organs and the specific effects on cytokine production offer a physiological basis for their immunomodulatory role in vivo.

机译：由于IL-12对细胞内病原体起着核心作用，并有助于免疫疾病的发病，因此其调节至关重要。这项研究检查了两种神经肽，血管活性肠肽（VIP）和垂体腺苷酸环化酶激活多肽（PACAP）对白介素12（IL-12）产生的影响。 VIP / PACAP剂量依赖性地抑制IL-12。 1型VIP受体（VPAC1）和2型VIP受体（VPAC2）主要通过cAMP / PKA途径介导IL-12的抑制。 VIP / PACAP可在内毒素血症小鼠体内抑制IL-12，IL-6，肿瘤坏死因子α（TNFalpha）和干扰素γ（IFNgamma）的产生。淋巴器官中VIP / PACAP的存在以及对细胞因子产生的特定作用为其体内免疫调节作用提供了生理基础。

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《Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology》 |1999年第2期|共15页
作者
Delgado M; Munoz Elias-EJ; Gomariz RP; Ganea D;
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正文语种 eng
中图分类神经病学与精神病学;医学免疫学;
关键词
Interleukin-12; Lipopolysaccharides; Macrophages; Peritoneal; Neuropeptides; 白细胞介素12; 脂多糖类; 巨噬细胞; 腹膜; 神经肽类; 血管活性肠肽;

机译：Interleukin-12;Lipopolysaccharides;Macrophages;Peritoneal;Neuropeptides;白细胞介素12;脂多糖类;巨噬细胞;腹膜;神经肽类;血管活性肠肽;

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1. VIP and PACAP inhibit IL-12 production in LPS-stimulated macrophages. Subsequent effect on IFNgamma synthesis by T cells. [J] . Delgado M, Munoz Elias-EJ, Gomariz RP, Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology . 1999,第2期

机译：VIP和PACAP抑制LPS刺激的巨噬细胞中IL-12的产生。 T细胞对IFNγ合成的后续影响。
2. LPS-stimulated SJL macrophages produce IL-12 and IL-18 that inhibit IgE production in vitro by induction of IFN-gamma production from CD3intIL-2R beta+ T cells. [J] . Yoshimoto T, Nagai N, Ohkusu K, The Journal of Immunology: Official Journal of the American Association of Immunologists . 1998,第3期

机译：LPS刺激的SJL巨噬细胞通过诱导CD3intIL-2Rβ+ T细胞产生的IFN-γ，在体外产生抑制IgE产生的IL-12和IL-18。
3. Interleukin 10 (IL-10) inhibits human lymphocyte interferon gamma-production by suppressing natural killer cell stimulatory factor/IL-12 synthesis in accessory cells. [J] . A DAndrea, M Aste-Amezaga, N M Valiante, The Journal of Experomental Medicine . 1993,第3期

机译：白细胞介素10（IL-10）通过抑制辅助细胞中的自然杀伤细胞刺激因子/ IL-12合成来抑制人淋巴细胞干扰素的产生。
4. Minocycline nano-liposome inhibit the production of TNF-α in LPS-stimulated macrophages [C] . Di Liu, Deyu Hu, Xue Li, Nanoelectronics Conference (INEC), 2010 . 2010

机译：米诺环素纳米脂质体抑制LPS刺激的巨噬细胞中TNF-α的产生
5. PART 1: SYNTHESIS OF IRREVERSIBLE INHIBITORS OF ALDOSE REDUCTASE WITH SUBSEQUENT DEVELOPMENT OF A CARBON-13 NMR PROTEIN PROBE. PART 2: SYNTHESIS OF SELENIUM ANALOGS OF DOPAMINE AS POTENTIAL DOPAMINE RECEPTOR AGONISTS. [D] . ARES, JEFFREY JOSEPH. 1986

机译：第1部分：合成具有碳13 NMR蛋白质探针的醛糖还原酶的不可逆抑制剂。第2部分：作为潜在的多巴胺受体激动剂的多巴胺硒类似物的合成。
6. Interleukin-18 (IFNgamma-inducing factor) induces IL-8 and IL-1beta via TNFalpha production from non-CD14+ human blood mononuclear cells. [O] . A J Puren, G Fantuzzi, Y Gu, 1998

机译：白介素-18（IFNγ诱导因子）通过从非CD14 +人血单核细胞产生TNFalpha诱导IL-8和IL-1beta。
7. Pro-oxidant activity of indicaxanthin from Opuntia ficus indica modulates arachidonate metabolism and prostaglandin synthesis through lipid peroxide production in LPS-stimulated RAW 264.7 macrophages. [O] . Allegra M, DAcquisto F, Tesoriere L, 2014

机译：来自印度仙人掌的印度洋黄嘌呤的促氧化活性通过在LPS刺激的RAW 264.7巨噬细胞中产生脂质过氧化物来调节花生四烯酸酯的代谢和前列腺素的合成。

VIP and PACAP inhibit IL-12 production in LPS-stimulated macrophages. Subsequent effect on IFNgamma synthesis by T cells.

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