The Host Cell Transcription Factor EGR1 Is Induced by Bacteria through the EGFR-ERK1/2 Pathway.
The Host Cell Transcription Factor EGR1 Is Induced by Bacteria through the EGFR-ERK1/2 Pathway.
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宿主细胞转录因子EGR1通过EGFR-ERK1/2途径诱导细菌诱导。
DOI：
10.3389/fcimb.2017.00016
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发表时间：
2017
影响因子：
5.7
通讯作者：
Jonsson AB
中科院分区：
文献类型：
--
作者：
de Klerk N;Saroj SD;Wassing GM;Maudsdotter L;Jonsson AB
细菌定植的第一步是粘附到宿主上皮细胞上。细菌粘连后的早期宿主反应仍知之甚少。早期生长反应1（EGR1）是一种早期反应转录调节因子，可以被各种环境刺激快速诱导。几种细菌可以诱导宿主细胞中 EGR1 的表达，但所涉及的细菌特征和这种反应的潜在分子机制在很大程度上尚不清楚。在这里，我们证明EGR1可以在宿主上皮细胞中被不同种类的细菌诱导，而与粘附水平、革兰氏染色类型和致病性无关。然而，细菌的活力和与宿主细胞的接触是必要的，这表明细菌和宿主之间的积极相互作用很重要。此外，在源自自然感染部位的细胞中观察到最强的反应，这表明 EGR1 诱导是细胞类型特异性的。最后，我们表明 EGFR-ERK1/2 和 β1-整合素信号传导是细菌介导的 EGR1 上调的主要途径。总之，上皮细胞中 EGR1 表达的增加是宿主与细菌相互作用时常见的应激诱导的细胞类型特异性反应，由 EGFR-ERK1/2 和 β1-整合素信号传导介导。
The essential first step in bacterial colonization is adhesion to the host epithelial cells. The early host-responses post-bacterial adhesions are still poorly understood. Early growth response 1 (EGR1) is an early response transcriptional regulator that can be rapidly induced by various environmental stimuli. Several bacteria can induce EGR1 expression in host cells, but the involved bacterial characteristics and the underlying molecular mechanisms of this response are largely unknown. Here, we show that EGR1 can be induced in host epithelial cells by different species of bacteria independent of the adherence level, Gram-staining type and pathogenicity. However, bacterial viability and contact with host cells is necessary, indicating that an active interaction between bacteria and the host is important. Furthermore, the strongest response is observed in cells originating from the natural site of the infection, suggesting that the EGR1 induction is cell type specific. Finally, we show that EGFR–ERK1/2 and β1-integrin signaling are the main pathways used for bacteria-mediated EGR1 upregulation. In conclusion, the increase of EGR1 expression in epithelial cells is a common stress induced, cell type specific response upon host-bacteria interaction that is mediated by EGFR–ERK1/2 and β1-integrin signaling.