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首页> 外文期刊>Journal of Reproductive Immunology >Interleukin-18 levels and mouse Leydig cell apoptosis during lipopolysaccharide-induced acute inflammatory conditions
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Interleukin-18 levels and mouse Leydig cell apoptosis during lipopolysaccharide-induced acute inflammatory conditions

机译：白细胞介素-18水平和小鼠Leydig细胞凋亡在脂多糖诱导的急性炎症条件下

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Interleukin (IL)-18 is an inflammasome-mediated cytokine produced by germ cells, Leydig cells, and resident macrophages that is indispensable in the maintenance of homeostasis in the testis. We previously demonstrated that endogenous IL-18 induces testicular germ cell apoptosis during acute inflammation when plasma IL-18 levels are very high. However, the impact of acute inflammation and IL-18 on Leydig cells remained unclear. TM3 cells, a mouse Leydig cell line, and RAW264.7 cells, a mouse macrophage cell line, were stimulated with lipopolysaccharide (LPS) or recombinant IL-18 (rIL-18). We assessed the expression of inflammatory cytokines, caspase cleavage, and markers of apoptotic pathways. In Leydig cells, caspase 3 cleavage was increased and death-receptor-mediated apoptotic pathways were activated after LPS stimulation. However, LPS stimulation did not increase IL-18 expression in the Leydig cell line. When high-dose rIL-18 was administered to the Leydig cell line to mimic levels seem after inflammation, rIL-18 upregulated Tnf-alpha mRNA, Fadd mRNA, and Fas protein, promoted cleavage of caspase-8 and caspase3, and induced apoptosis. Low-dose rIL-18 did not stimulate apoptosis. To determine if the high level of IL-18 seen in the testes after inflammation was derived from immune cells, we examined IL-18 protein expression in a macrophage cell line, RAW264.7. In contrast to the TM3 cells, IL-18 was significantly increased in RAW264.7 cells after LPS stimulation. These results suggest that high-dose IL-18 derived from macrophages is harmful to Leydig cells. Reducing the overexpression of IL-18 could be a new therapeutic approach to prevent Leydig cell apoptosis as a result of acute inflammation.
机译：白细胞介素（IL）-18是一种炎症体介导的细胞因子，由生殖细胞、睾丸间质细胞和常驻巨噬细胞产生，在维持睾丸内环境稳定中不可或缺。我们之前已经证明，当血浆IL-18水平非常高时，内源性IL-18在急性炎症期间诱导睾丸生殖细胞凋亡。然而，急性炎症和IL-18对睾丸间质细胞的影响尚不清楚。小鼠睾丸间质细胞系TM3细胞和RAW264。用脂多糖（LPS）或重组IL-18（rIL-18）刺激小鼠巨噬细胞系7个细胞。我们评估了炎性细胞因子的表达、半胱天冬酶的裂解和凋亡途径的标志物。在Leydig细胞中，在LPS刺激后，caspase 3裂解增加，死亡受体介导的凋亡途径被激活。然而，LPS刺激并没有增加睾丸间质细胞系中IL-18的表达。当给Leydig细胞系注射高剂量rIL-18以模拟炎症后的水平时，rIL-18上调Tnf-αmRNA、Fadd mRNA和Fas蛋白，促进caspase-8和caspase-3的切割，并诱导细胞凋亡。低剂量rIL-18不刺激细胞凋亡。为了确定炎症后睾丸中高水平的IL-18是否来自免疫细胞，我们检测了巨噬细胞系RAW264中的IL-18蛋白表达。7.与TM3细胞相比，RAW264中的IL-18显著增加。LPS刺激后的7个细胞。这些结果表明，来自巨噬细胞的高剂量IL-18对睾丸间质细胞有害。减少IL-18的过度表达可能是防止急性炎症导致睾丸间质细胞凋亡的一种新的治疗方法。

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    Inoue Taketo; Aoyama-Ishikawa Michiko; Uemura Mikiko; Yamashita Hayato; Koga Yuka; Terashima Mariko; Usami Makoto; Kotani Joji; Hirata Junichi;

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    Hyogo Coll Med Dept Emergency Disaster &

    Crit Care Med 1-1 Mukogawa Cho Nishinomiya Hyogo;

    Hyogo Coll Med Dept Emergency Disaster &

    Crit Care Med 1-1 Mukogawa Cho Nishinomiya Hyogo;

    Kansai Univ Welf Sci Fac Hlth Sci Dept Rehabil 3-11-1 Asahigaoka Kashiwara Osaka 5820026 Japan;

    Kobe Univ Dept Biophys Grad Sch Hlth Sci Suma Ku 7-10-2 Tomogaoka Kobe Hyogo 6540142 Japan;

    Kobe Univ Dept Biophys Grad Sch Hlth Sci Suma Ku 7-10-2 Tomogaoka Kobe Hyogo 6540142 Japan;

    Hyogo Coll Med Dept Emergency Disaster &

    Crit Care Med 1-1 Mukogawa Cho Nishinomiya Hyogo;

    Konan Womens Univ Dept Clin Nutr &

    Dietet Higashinada Ku 6-2-23 Morikita Machi Kobe Hyogo;

    Kobe Univ Dept Surg Related Div Disaster &

    Emergency Med Grad Sch Med Chuo Ku 7-5-2 Kusunocho;

    Hyogo Coll Med Dept Emergency Disaster &

    Crit Care Med 1-1 Mukogawa Cho Nishinomiya Hyogo;

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  • 正文语种 eng
  • 中图分类 妇科学;
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