Role of GATA transcription factor ELT-2 and p38 MAPK PMK-1 in recovery from acute P. aeruginosa infection in C. elegans.

Role of GATA transcription factor ELT-2 and p38 MAPK PMK-1 in recovery from acute P. aeruginosa infection in C. elegans.
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DOI:
10.1080/21505594.2016.1222334
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发表时间:
2017-04-03
期刊:
影响因子:
5.2
通讯作者:
Aballay A
Aballay A
中科院分区:
生物学2区
文献类型:
--
作者:
Head BP;Olaitan AO;Aballay A

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由细菌病原体引起的传染病降低了其相关宿主的适应性,但通常持续时间有限。为了使患病宿主在恢复时恢复任何失去的健康,必须采用各种分子、细胞和生理过程。为了更好地理解恢复过程的机制,我们模拟了急性铜绿假单胞菌感染的C。线虫使用短暂暴露于这种病原体和随后的抗生素治疗。为了鉴定铜绿假单胞菌感染恢复期间改变的宿主基因,我们进行了全基因组表达谱分析。对该数据集的分析表明,宿主免疫系统的活性在恢复后下调,并在恢复期间显示出共有的和病原体特异性的宿主应答。我们确定加塔转录因子ELT-2和p38 MAP激酶PMK-1是动物从急性铜绿假单胞菌感染中成功恢复所必需的。此外,我们发现ELT-2在恢复过程中比PMK-1发挥更突出和更早的作用。我们的数据进一步阐明了从急性细菌感染中恢复所涉及的分子机制和转录程序,这提供了对整个感染性疾病过程的更好理解。
Infectious diseases caused by bacterial pathogens reduce the fitness of their associated host but are generally limited in duration. In order for the diseased host to regain any lost fitness upon recovery, a variety of molecular, cellular, and physiological processes must be employed. To better understand mechanisms underlying the recovery process, we have modeled an acute Pseudomonas aeruginosa infection in C. elegans using brief exposures to this pathogen and subsequent antibiotic treatment. To identify host genes altered during recovery from P. aeruginosa infection, we performed whole genome expression profiling. The analysis of this dataset indicated that the activity of the host immune system is down-regulated upon recovery and revealed shared and pathogen-specific host responses during recovery. We determined that the GATA transcription factor ELT-2 and the p38 MAP kinase PMK-1 are necessary for animals to successfully recover from an acute P. aeruginosa infection. In addition, we found that ELT-2 plays a more prominent and earlier role than PMK-1 during recovery. Our data sheds further light on the molecular mechanisms and transcriptional programs involved in recovery from an acute bacterial infection, which provides a better understanding of the entire infectious disease process.