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首页> 外文期刊>Fish & Shellfish Immunology >Dietary choline deficiency and excess induced intestinal inflammation and alteration of intestinal tight junction protein transcription potentially by modulating NF-kappa B, STAT and p38 MAPK signaling molecules in juvenile Jian carp
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Dietary choline deficiency and excess induced intestinal inflammation and alteration of intestinal tight junction protein transcription potentially by modulating NF-kappa B, STAT and p38 MAPK signaling molecules in juvenile Jian carp

机译:膳食胆碱缺乏和过量诱导的肠道炎症以及可能通过调节幼年健鲤中的NF-κB,STAT和p38 MAPK信号分子而改变肠道紧密连接蛋白的转录

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摘要

This study investigated the effects of choline on intestinal mucosal immune and the possible mechanisms in fish by feeding juvenile Jian carp (Cyprinus carpio var. Jian) with graded levels of dietary choline (165-1820 mg/kg diet) for 65 days. The results firstly showed that choline deficiency induced inflammatory infiltration in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) of fish. Meanwhile, compared with the optimal choline group, choline deficiency decreased the activities of lysozyme and acid phosphatase, contents of complement 3 and IgM in the intestine, downregulated the mRNA levels of antimicrobial peptides (liver-expressed antimicrobial peptide (LEAP) 2A and defensin-3 in the PI and MI, LEAP-2B and hepcidin in the PI, MI and DI), anti-inflammatory cytokines (interleukin (IL) 10 and transforming growth factor beta 2 in the PI, MI and DI), and signaling molecule I kappa B in the PI, MI and DI; while upregulated the mRNA levels of pro-inflammatory cytokines (IL-6a and tumor necrosis factor a in the MI and DI, interferon gamma 2b in the PI and MI, IL-1 beta and IL-6b in the PI, MI and DI), and signaling molecules (Toll-like receptor 4 in the MI, myeloid differentiation primary response 88 in the PI and MI, Janus kinase 3 and tyrosine kinase 2 in the MI and DI, nuclear factor kappa B (NF-kappa B), signal transducers and activators of transcription (STAT) 4 and STAT5 in the PI, MI and DI) of juvenile Jian carp, further indicating that choline deficiency caused inflammation and immunity depression in the intestine of fish. But choline deficiency decreased the PI IL-6a mRNA level, and increased the DI LEAP-2A and defensin-3 mRNA levels with unknown reasons. Furthermore, dietary choline deficiency downregulated mRNA levels of tight junction (TJ) proteins (claudin 3c in the PI and MI, claudin 7, claudin 11 and occludin in the PI, MI and DI) and signaling molecule mitogen-activated protein kinases p38 in the PI, MI and DI of juvenile Jian carp, whereas upregulated the mRNA levels of claudin 3b in the MI and DI, and claudin 3c in the DI. Moreover, the excessive choline exhibited negative effects on intestinal immunity and TJ proteins that were similar to the choline deficiency. In summary, dietary choline deficiency or excess caused the depression of intestinal mucosal immune by inducing inflammation and dysfunction of the intestinal physical barrier, and regulating related signaling molecules of fish. (C) 2016 Elsevier Ltd. All rights reserved.
机译:本研究通过给幼年Jian鲤(Cyprinus carpio var。Jian)喂食分级水平的日粮胆碱(165-1820 mg / kg日粮)65天,研究了胆碱对鱼肠粘膜免疫的影响及其可能的机制。结果首先表明胆碱缺乏引起鱼近端肠(PI),中肠(MI)和远端肠(DI)的炎症浸润。同时,与最佳胆碱组相比,胆碱缺乏会降低肠道中的溶菌酶和酸性磷酸酶活性,补体3和IgM的含量,下调抗菌肽(肝表达的抗菌肽(LEAP)2A和防御素-mRNA)的mRNA水平。 PI和MI中为3,PI,MI和DI中为LEAP-2B和hepcidin),抗炎细胞因子(PI,MI和DI中为白介素(IL)10和转化生长因子β2),以及信号分子I PI,MI和DI中的Kappa B;同时上调促炎性细胞因子的mRNA水平(MI和DI中的IL-6a和肿瘤坏死因子a,PI和MI中的干扰素gamma 2b,PI,MI和DI中的IL-1 beta和IL-6b)以及信号分子(MI中的Toll样受体4,PI和MI中的髓样分化主要反应88,MI和DI中的Janus激酶3和酪氨酸激酶2,核因子κB(NF-κB),信号幼Jian鱼的PI,MI和DI中的转录和激活转录因子(STAT)4和STAT5,进一步表明胆碱缺乏导致鱼肠发炎和免疫力下降。但胆碱缺乏会降低PI IL-6a mRNA水平,并增加DI LEAP-2A和Defensin-3 mRNA水平,原因不明。此外,饮食中胆碱缺乏会下调紧密连接(TJ)蛋白的mRNA水平(PI和MI中的claudin 3c,PI,MI和DI中的claudin 7,claudin 11和occludin)和信号转导分子促分裂原活化蛋白激酶p38。 Jian鱼的PI,MI和DI,而MI和DI中的claudin 3b和DI中的claudin 3c的mRNA水平上调。而且,过量的胆碱对肠免疫和TJ蛋白表现出负面影响,类似于胆碱缺乏。总之,饮食中胆碱缺乏或过量会引起肠道粘膜屏障的炎症和功能紊乱,并调节鱼类的相关信号分子,从而导致肠道粘膜免疫功能下降。 (C)2016 Elsevier Ltd.保留所有权利。

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