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首页> 外文期刊>Cellular immunology >Cytochrome P450 1A1 enhances Arginase-1 expression, which reduces LPS-induced mouse peritonitis by targeting JAK1/STAT6
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Cytochrome P450 1A1 enhances Arginase-1 expression, which reduces LPS-induced mouse peritonitis by targeting JAK1/STAT6

机译：细胞色素P450 1A1增强了氨基酶-1表达，其通过靶向JAK1 / Stat6降低LPS诱导的小鼠腹膜炎

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摘要

The polarization of macrophages is critical to inflammation and tissue repair, with unbalanced macrophage polarization associated with critical dysfunctions of the immune system. Cytochrome P450 1A1 (CYP1A1) is a hydroxylase mainly controlled by the inflammation-limiting aryl hydrocarbon receptor (AhR), which plays a critical role in mycoplasma infection, oxidative stress injury, and cancer. Arginase-1 (Arg-1) is a surrogate for polarized alternative macrophages and is important to the production of nitric oxide (NO) by the modulation of arginine. In the present study, we found CYP1A1 to be upregulated in IL-4-stimulated mouse peritoneal macrophages (PMs) and human peripheral blood monocytes. Using CYP1A1-overexpressing RAW264.7 cells (CYP1A1/RAW) we found that CYP1A1 augmented Arg-1 expression by strengthening the activation of the JAK1/STAT6 signaling pathway in macrophages treated with IL-4. 15(S)-HETE, a metabolite of CYP1A1 hydroxylase, was elevated in IL-4-induced CYP1A1/RAW cells. Further, in macrophages, the loss-of-CYP1A1-hydroxylase activity was associated with reduced IL-4-induced Arg-1 expression due to impaired 15(S)-HETE generation. Of importance, CYP1A1 overexpressing macrophages reduced the inflammation associated with LPS-induced peritonitis. Taken together, these findings identified a novel signaling axis, CYP1A1-15(S)-HETE-JAK1-STAT6, that may be a promising target for the proper maintenance of macrophage polarization and may also be a means by which to treat immune-related disease due to macrophage dysfunction.
机译：巨噬细胞的极化对炎症和组织修复至关重要，与免疫系统的临界功能障碍相关的不平衡巨噬细胞极化。细胞色素P450 1A1（CYP1A1）是主要由炎症限制芳基烃受体（AHR）控制的羟化物，其在支原体感染，氧化应激损伤和癌症中起着关键作用。 Aginase-1（Arg-1）是替代偏振型巨噬细胞的替代物，并且通过精氨酸的调节来生产一氧化氮（NO）。在本研究中，我们发现CYP1A1在IL-4刺激的小鼠腹膜巨噬细胞（PMS）和人外周血单核细胞中升高。使用CYP1A1-过度抑制RAW264.7细胞（CYP1A1 / RAW），我们发现CYP1A1通过加强用IL-4处理的巨噬细胞激活JAK1 / Stat6信号传导途径的激活来增强ARG-1。 15（s） - 肝脏代谢物，CYP1A1羟化酶的代谢物在IL-4诱导的CYP1A1 /原料细胞中升高。此外，在巨噬细胞中，由于15（s）的生成受损，CYP1A1-羟化酶活性与IL-4诱导的ARG-1表达有关。重要性，过表达巨噬细胞的CYP1A1减少了与LPS诱导的腹膜炎相关的炎症。这些发现鉴定了一种新型信号轴CYP1A1-15（S）-HET-JAK1-STAT6，其可能是适当维持巨噬细胞极化的有希望的靶标，也可以是治疗免疫相关的手段由于巨噬细胞功能障碍引起的疾病。

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  • 来源
    《Cellular immunology》 |2020年第1期|共11页
  • 作者

    Tian Li-Xing; Tang Xin; Zhu Jun-Yu; Zhang Wei; Tang Wan-Qi; Yan Jun; Xu Xiang; Liang Hua-Ping;

  • 作者单位

    Army Med Univ Daping Hosp Dept Wound Infect &

    Drug State Key Lab Trauma Burns &

    Combined Injury;

    Army Med Univ Daping Hosp Dept Wound Infect &

    Drug State Key Lab Trauma Burns &

    Combined Injury;

    Army Med Univ Daping Hosp Dept Wound Infect &

    Drug State Key Lab Trauma Burns &

    Combined Injury;

    Hainan Med Univ Emergency &

    Trauma Coll Xueyuan Rd 3 Haikou Hainan Peoples R China;

    Army Med Univ Daping Hosp Dept Wound Infect &

    Drug State Key Lab Trauma Burns &

    Combined Injury;

    Army Med Univ Daping Hosp Dept Wound Infect &

    Drug State Key Lab Trauma Burns &

    Combined Injury;

    Army Med Univ Daping Hosp Dept Wound Infect &

    Drug State Key Lab Trauma Burns &

    Combined Injury;

    Army Med Univ Daping Hosp Dept Wound Infect &

    Drug State Key Lab Trauma Burns &

    Combined Injury;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    Cytochrome P450 1A1; Arginase-1; Macrophage; Peritonitis;

    机译：细胞色素p450 1a1;氨基酶-1;巨噬细胞;腹膜炎;

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