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首页> 外文期刊>Environmental Pollution >Microcystin-leucine arginine exhibits immunomodulatory roles in testicular cells resulting in orchitis
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Microcystin-leucine arginine exhibits immunomodulatory roles in testicular cells resulting in orchitis

机译：微囊藻氨酸亮氨酸精氨酸在睾丸细胞中表现出免疫调节作用，导致睾丸炎

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摘要

Microcystin-leucine arginine (MC-LR) causes testicular inflammation and hinders spermatogenesis. However, the molecular mechanisms underlying the immune responses to MC-LR in the testis have not been elucidated in detail. In this study, we show that MC-LR induced immune responses in Sertoli cells (SC), germ cells (GC), and Leydig cells (LC) via activating phosphatidylinositol 3-kinase (PI3K)/AKTuclear factor kappa B (NF-kappa B), resulting in the production of pro-inflammatory cytokines and chemokines including tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and chemokine (C-X-C motif) ligand 10 (CXCL10). The observed effects were attributed to reduced activity of protein phosphatases 2A (PP2A) as a result of binding of MC-LR to the catalytic subunit of PP2A in SC and GC. By contrast, innate immune responses were triggered by Toll-like receptor 2 (TLR2) in LC because MC-LR could not enter into the LC and subsequently inhibit the PP2A activity. PI3K/AKT/NF-kappa B were also activated in SC, GC, and LC in vivo, with the enrichment of TNF-a, IL-6, MCP-1, and CXCL10 in the testis. Following chronic exposure, MC-LR-treated mice exhibited decreased sperm counts and abnormal sperm morphology. Our data demonstrate that MC-LR can activate innate immune responses in testicular cells, which provides novel insights to explore the mechanism associated with MC-LR-induced orchitis. (C) 2017 Elsevier Ltd. All rights reserved.
机译：微囊藻氨酸亮氨酸精氨酸（MC-LR）引起睾丸发炎并阻碍精子发生。然而，尚未详细阐明睾丸中针对MC-LR的免疫反应的分子机制。在这项研究中，我们表明MC-LR通过激活磷脂酰肌醇3-激酶（PI3K）/ AKT /核因子κB（NF）诱导了支持细胞（SC），生殖细胞（GC）和Leydig细胞（LC）的免疫应答-κB），导致促炎性细胞因子和趋化因子的产生，包括肿瘤坏死因子α（TNF-alpha），白介素6（IL-6），单核细胞趋化蛋白1（MCP-1）和趋化因子（ CXC基序）配体10（CXCL10）。观察到的效果归因于蛋白磷酸酶2A（PP2A）的活性降低，这是由于MC-LR与SC和GC中PP2A的催化亚基结合所致。相比之下，LC中的Toll样受体2（TLR2）触发了先天性免疫应答，因为MC-LR无法进入LC并随后抑制PP2A活性。 PI3K / AKT /NF-κB也在体内SC，GC和LC中激活，并在睾丸中富集TNF-a，IL-6，MCP-1和CXCL10。长期暴露后，经MC-LR处理的小鼠表现出精子数量减少和精子形态异常。我们的数据表明，MC-LR可以激活睾丸细胞的先天免疫应答，这为探索与MC-LR诱导的睾丸炎相关的机制提供了新的见解。 （C）2017 Elsevier Ltd.保留所有权利。

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  • 来源
    《Environmental Pollution》 |2017年第10期|964-975|共12页
  • 作者

    Chen Yabing; Wang Jing; Zhang Qin; Xiang Zou; Li Dongmei; Han Xiaodong;

  • 作者单位

    Nanjing Univ, Med Sch, Immunol & Reprod Biol Lab, State Key Lab Analyt Chem Life Sci, Nanjing 210093, Jiangsu, Peoples R China|Nanjing Univ, Jiangsu Key Lab Mol Med, Nanjing 210093, Jiangsu, Peoples R China;

    Nanjing Univ, Med Sch, Immunol & Reprod Biol Lab, State Key Lab Analyt Chem Life Sci, Nanjing 210093, Jiangsu, Peoples R China|Nanjing Univ, Jiangsu Key Lab Mol Med, Nanjing 210093, Jiangsu, Peoples R China;

    Nanjing Univ, Med Sch, Immunol & Reprod Biol Lab, State Key Lab Analyt Chem Life Sci, Nanjing 210093, Jiangsu, Peoples R China|Nanjing Univ, Jiangsu Key Lab Mol Med, Nanjing 210093, Jiangsu, Peoples R China;

    Hong Kong Polytech Univ, Fac Hlth & Social Sci, Dept Hlth Technol & Informat, Kowloon, Hong Kong, Peoples R China;

    Nanjing Univ, Med Sch, Immunol & Reprod Biol Lab, State Key Lab Analyt Chem Life Sci, Nanjing 210093, Jiangsu, Peoples R China|Nanjing Univ, Jiangsu Key Lab Mol Med, Nanjing 210093, Jiangsu, Peoples R China;

    Nanjing Univ, Med Sch, Immunol & Reprod Biol Lab, State Key Lab Analyt Chem Life Sci, Nanjing 210093, Jiangsu, Peoples R China|Nanjing Univ, Jiangsu Key Lab Mol Med, Nanjing 210093, Jiangsu, Peoples R China;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    Microcystin-LR; Immune responses; Testicular cells; Orchitis;

    机译：微囊藻毒素-LR;免疫反应;睾丸细胞;睾丸炎;

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