秀丽隐杆线虫Kruppel样转录因子KLF-1抑制固有免疫反应的机制研究
首发时间:2021-04-14
摘要:固有免疫(Innate immunity)是生物对抗病原体入侵的重要防御机制。然而,相关调控机制尚不完全清除。为了在已有基础上进一步探索秀丽隐杆线虫固有免疫的调控机制,实验构建了铜绿假单胞菌(Pseudomonas aeruginosa, PA14)和秀丽隐杆线虫(Caenorhabditis elegans , C.elegans)的病原-宿主模型,经转录组测序发现,铜绿假单胞菌处理秀丽隐杆线虫可以上调Kruppel样转录因子KLF-1的表达,提示KLF-1可能参与了线虫肠道固有免疫反应。进一步研究表明,抑制klf-1表达可增强p38/PMK-1信号通路下游免疫基因表达,进而提高线虫对PA14的耐受能力。因此,KLF-1可能是一种新的固有免疫抑制因子。
关键词: klf-1 p38/PMK-1 固有免疫 铜绿假单胞菌 秀丽隐杆线虫
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The genetic mechanism of Kruppel-like transcription factors KLF-1 suppressing innate immunity in Caenorhabditis elegans
Abstract: Innate immunity is the vital defense line against pathogens in organisms. However, the mechanism remains poorly understood. The aim of this study was to explore the factors affecting innate immunity of Caenorhabditis elegans (C. elegans) by using a pathogen and host model system in which C. elegans is killed by infecting with an opportunistic pathogen Pseudomonas aeruginosa (PA14). The RNA sequencing revealed that klf-1 gene encoding Kruppel-like transcription factor is significantly upregulated upon PA14 exposure, suggesting KLF-1 play a role in the C. elegans innate immunity. Inhibition of KLF-1 increases the resistance of C.elegans to PA14 infection and induces the expression of PMK-1-dependent downstream immune genes. Our further data support that the transcription factor KLF-1 negatively regulates the innate immunity of C. elegans via PMK-1 pathway. Therefore,KLF-1 may be a novel immunosuppressor.
Keywords: klf-1 p38/PMK-1 innate immunity Pseudomonas aeruginosa 14 Caenorhabditis elegans
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