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猪肺炎支原体暴露于过氧化氢后的全转录组分析

Global transcriptional analysis of Mycoplasma hyopneumoniae following exposure to hydrogen peroxide.

作者信息

Schafer Erin R, Oneal Michael J, Madsen Melissa L, Minion F Chris

机构信息

Department of Veterinary Microbiology and Preventive Medicine, Iowa State University, Ames, IA 50011, USA.

出版信息

Microbiology (Reading). 2007 Nov;153(Pt 11):3785-3790. doi: 10.1099/mic.0.2007/011387-0.

Abstract

Mycoplasma hyopneumoniae, the causative agent of swine enzootic pneumonia, colonizes the cilia of swine lungs, causing ciliostasis and cell death. M. hyopneumoniae is a component of the porcine respiratory disease complex (PRDC) and is especially problematic for the finishing swine industry, causing the loss of hundreds of millions of dollars in farm revenues worldwide. For successful infection, M. hyopneumoniae must effectively resist oxidative stresses due to the release of oxidative compounds from neutrophils and macrophages during the host's immune response. However, the mechanism that M. hyopneumoniae uses to avert the host response is still unclear. To gain a better understanding of the transcriptional responses of M. hyopneumoniae under oxidative stress, cultures were grown to early exponential phase and exposed to 0.5% hydrogen peroxide for 15 min. RNA samples from these cultures were collected and compared to RNA samples from control cultures using two-colour PCR-based M. hyopneumoniae microarrays. This study revealed significant downregulation of important glycolytic pathway genes and gene transcription proteins, as well as a protein known to activate oxidative stressor cascades in neutrophils. Sixty-nine per cent of the upregulated genes were hypothetical with no known function. This study has also revealed significantly differentially expressed genes common to other environmental stress responses, indicating that further investigation of universal stress response genes of M. hyopneumoniae is merited.

摘要

猪肺炎支原体是猪地方流行性肺炎的病原体,它定殖于猪肺的纤毛上,导致纤毛运动停滞和细胞死亡。猪肺炎支原体是猪呼吸道疾病综合征(PRDC)的一个组成部分,对育肥猪产业尤其成问题,在全球范围内给养殖场收入造成数亿美元的损失。为了成功感染,猪肺炎支原体必须有效抵抗氧化应激,因为在宿主免疫反应期间中性粒细胞和巨噬细胞会释放氧化化合物。然而,猪肺炎支原体用于规避宿主反应的机制仍不清楚。为了更好地了解猪肺炎支原体在氧化应激下的转录反应,将培养物培养至早期指数期,并用0.5%过氧化氢处理15分钟。收集这些培养物的RNA样本,并使用基于双色PCR的猪肺炎支原体微阵列与对照培养物的RNA样本进行比较。这项研究揭示了重要糖酵解途径基因和基因转录蛋白以及一种已知可激活中性粒细胞氧化应激级联反应的蛋白的显著下调。上调基因中有69%是功能未知的假设基因。这项研究还揭示了其他环境应激反应中共同存在的显著差异表达基因,表明值得对猪肺炎支原体的普遍应激反应基因进行进一步研究。

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