Effects of strains of Lactococcus lactis on the production of nitric oxide and cytokines in murine macrophages

Effects of strains of Lactococcus lactis on the production of nitric oxide and cytokines in murine macrophages
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乳酸乳球菌菌株对小鼠巨噬细胞一氧化氮和细胞因子产生的影响

DOI:
10.1007/s10753-014-9901-6
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发表时间:
2014
期刊:
影响因子:
5.1
通讯作者:
Mizumachi K.
Mizumachi K.
中科院分区:
医学2区
文献类型:
--
作者:
Suzuki C;Aoki-Yoshida A;Kimoto-Nira H;Kobayashi M;Sasaki K;Mizumachi K.

文献摘要

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一氧化氮(NO)是一种多功能介质,参与多种病理生理过程。乳酸菌(LAB)对诱导型一氧化氮合酶(INOS)诱导宿主胃肠道免疫反应的影响研究较少,尤其是乳制品中使用的乳酸乳球菌。我们调查了他们的能力。乳酸菌在小鼠巨噬细胞样细胞系J774.1和小鼠腹膜巨噬细胞中诱导NO合成。NO诱导的程度是特异的。使用的是乳酸菌。与未处理对照相比,L。乳细胞可降低NO和肿瘤坏死因子-α水平,但进一步刺激白细胞介素12的产生。添加L。乳细胞对巨噬细胞的刺激作用呈剂量依赖性地增加NO和IL-10的产生,降低IL-12p70的产生。添加L。乳细胞对干扰素-γ刺激的J774.1细胞的死亡增加,NO和IL-12p40的产生增加,而加入诱导型一氧化氮合酶的特异性抑制剂1400W则减少NO的产生和细胞死亡。相反,在J774.1细胞中加入1400W进一步增加了IL-12p40的产生,这表明IL-12的产生受到过量内源性NO的干扰。IL-12的产生被认为是免疫刺激作用改善的一个标志。我们的结果表明,通过限制内源性NO的产生可以增加IL-12的产生。
Nitric oxide (NO) is a multifunctional mediator that is involved in a variety of pathologic and physiologic processes. Few studies have addressed the effect of lactic acid bacteria (LAB), especiallyLactococcus lactisstrains used in dairy products, on inducible nitric oxide synthase (iNOS) induction as a component of the host’s gastrointestinal immune response. We investigated the ability ofL. lactisstrains to induce NO synthesis in the murine macrophage-like cell line J774.1 and in peritoneal macrophages from mice. The degree of NO induction was specific to theL. lactisstrain used. Compared with the no-treatment control, heat treatment ofL. lactiscells decreased NO and TNF-α levels but further stimulated interleukin (IL)-12 production. AddingL. lactiscells to peritoneal macrophages dose-dependently increased the production of NO and IL-10 but decreased that of IL-12p70. AddingL. lactiscells to interferon-γ-stimulated J774.1 cells enhanced cell death and the production of NO and IL-12p40, whereas addition of 1400W, a specific inhibitor of iNOS, decreased NO production and cell death. Conversely, adding 1400W to J774.1 cells further enhanced IL-12p40 production, suggesting that IL-12 production is perturbed by excess endogenous NO. IL-12 production is thought to be a marker of improved immunostimulation. Our results suggest that IL-12 production could be increased by limiting endogenous NO production.