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首页> 外文期刊>American Journal of Physiology >Soluble factors from Lactobacillus GG activate MAPKs and induce cytoprotective heat shock proteins in intestinal epithelial cells.
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Soluble factors from Lactobacillus GG activate MAPKs and induce cytoprotective heat shock proteins in intestinal epithelial cells.

机译：来自乳杆菌GG的可溶性因子激活MAPK并在肠上皮细胞中诱导细胞保护性热休克蛋白。

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摘要

Conditioned media from the probiotic Lactobacillus GG (LGG-CM) induce heat shock protein (Hsp) expression in intestinal epithelial cells. LGG-CM induces both Hsp25 and Hsp72 in a time- and concentration-dependent manner. These effects are mediated by a low-molecular-weight peptide that is acid and heat stable. DNA microarray experiments demonstrate that Hsp72 is one of the most highly upregulated genes in response to LGG-CM treatment. Real-time PCR and electrophoretic mobility shift assay confirm that regulation of Hsp induction is at least in part transcriptional in nature, involving heat shock factor-1. Although Hsps are not induced for hours after exposure, transient exposure to LGG-CM is sufficient to initiate the signal for Hsp induction, suggesting that signal transduction pathways may be involved. Experiments confirm that LGG-CM modulates the activity of certain signaling pathways in intestinal epithelial cells by activating MAP kinases. Inhibitors of p38 and JNK block the expression of Hsp72 normally induced by LGG-CM. Functional studies indicate that LGG-CM treatment of gut epithelial cells protects them from oxidant stress, perhaps by preserving cytoskeletal integrity. By inducing the expression of cytoprotective Hsps in gut epithelial cells, and by activating signal transduction pathways, the peptide product(s) secreted by LGG may contribute to the beneficial clinical effects attributed to this probiotic.
机译：益生菌乳杆菌GG（LGG-CM）的条件培养基在肠上皮细胞中诱导热休克蛋白（Hsp）表达。 LGG-CM以时间和浓度依赖性方式诱导Hsp25和Hsp72。这些作用是由酸和热稳定的低分子量肽介导的。 DNA微阵列实验表明，Hsp72是响应LGG-CM处理的最高度上调的基因之一。实时PCR和电​​泳迁移率变动分析证实，Hsp诱导的调控至少部分是转录，涉及热休克因子-1。尽管在暴露后数小时内未诱导出Hsps，但短暂暴露于LGG-CM足以引发Hsp诱导信号，表明可能涉及信号转导途径。实验证实，LGG-CM通过激活MAP激酶来调节肠道上皮细胞中某些信号通路的活性。 p38和JNK抑制剂可阻断LGG-CM正常诱导的Hsp72表达。功能研究表明，LGG-CM处理肠道上皮细胞可以保护其免受氧化应激，也许是通过保持细胞骨架的完整性。通过在肠道上皮细胞中诱导细胞保护性Hsps的表达，并通过激活信号转导途径，LGG分泌的肽产物可能有助于归因于这种益生菌的有益临床效果。

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