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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >The dietary histone deacetylase inhibitor sulforaphane induces human beta-defensin-2 in intestinal epithelial cells.
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The dietary histone deacetylase inhibitor sulforaphane induces human beta-defensin-2 in intestinal epithelial cells.

机译：饮食中的组蛋白脱乙酰基酶抑制剂萝卜硫素可在肠上皮细胞中诱导人β-防御素2。

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Antimicrobial peptides like human beta-defensin-2 (HBD-2) play an important role in the innate immune system protecting the intestinal mucosa against bacterial invasion. The dietary histone deacetylase (HDAC) inhibitors sulforaphane (SFN) and butyrate have received a great deal of attention because of their ability to simultaneously modulate multiple cellular targets involved in cellular protection. In this study the influence of SFN and butyrate on HBD-2 expression as well as the molecular pathways involved in SFN-mediated induction of HBD-2 were scrutinized. Treatment of Caco-2, HT-29 and SW480 cells with SFN led to a time- and dose-dependent upregulation of HBD-2 mRNA expression as determined by semi-quantitative reverse transcription-polymerase chain reaction. Moreover, HBD-2 protein production increased in response to SFN, measured by enzyme-linked immunosorbent assay. Induction of HBD-2 was also observed in response to butyrate. Immunofluorescence analysis revealed that the protein was localized in the cytosol. Coincubation of SFN with a vitamin D receptor (VDR), or an extracellular-regulated kinase 1/2 or a nuclear factor-kappaB inhibitor all reduced HBD-2 mRNA upregulation. In contrast, transfection of cells with a dominant-negative peroxisome proliferator-activated receptor gamma (PPARgamma) mutant vector to inhibit PPARgamma wild-type action and inhibition of p38 mitogen-activated protein kinase (MAPK) signalling did not affect SFN-mediated upregulation of HBD-2 mRNA. Moreover, SFN induced the expression of VDR, PPARgamma and phosphorylated ERK1/2 but did not affect p38 MAPK activation. The data clearly demonstrate for the first time that the dietary HDAC inhibitor SFN is able to induce antimicrobial peptides in colonocytes. In this process HBD-2 expression is regulated via VDR, mitogen-activated protein kinase kinase/extracellular-regulated kinase and nuclear factor-kappaB signalling.
机译：诸如人β-防御素2（HBD-2）之类的抗菌肽在先天免疫系统中保护肠粘膜免受细菌入侵具有重要作用。饮食组蛋白脱乙酰基酶（HDAC）抑制剂萝卜硫烷（SFN）和丁酸酯因其能够同时调节参与细胞保护作用的多个细胞靶标而备受关注。在这项研究中，仔细研究了SFN和丁酸酯对HBD-2表达的影响以及SFN介导的HBD-2诱导的分子途径。用SFN处理Caco-2，HT-29和SW480细胞会导致HBD-2 mRNA表达的时间和剂量依赖性上调，这是通过半定量逆转录聚合酶链反应确定的。此外，通过酶联免疫吸附测定法测定，响应SFN，HBD-2蛋白的产量增加。还观察到了响应丁酸的HBD-2的诱导。免疫荧光分析表明该蛋白位于细胞质中。 SFN与维生素D受体（VDR）或细胞外调节的激酶1/2或核因子-κB抑制剂的共孵育均减少了HBD-2 mRNA的上调。相反，用显性负过氧化物酶体增殖物激活的受体γ（PPARgamma）突变载体转染细胞以抑制PPARgamma野生型作用并抑制p38丝裂原激活的蛋白激酶（MAPK）信号转导并不影响SFN介导的上调。 HBD-2 mRNA。此外，SFN诱导VDR，PPARγ和磷酸化ERK1 / 2的表达，但不影响p38 MAPK激活。数据清楚地首次证明，饮食HDAC抑制剂SFN能够诱导结肠细胞中的抗菌肽。在这个过程中，HBD-2的表达通过VDR，有丝分裂原激活的蛋白激酶激酶/细胞外调节激酶和核因子-κB信号传导来调节。

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