Oneal Michael J, Schafer Erin R, Madsen Melissa L, Minion F Chris
Department of Veterinary Microbiology and Preventive Medicine, Iowa State University, Ames, IA 50011, USA.
Microbiology (Reading). 2008 Sep;154(Pt 9):2581-2588. doi: 10.1099/mic.0.2008/020230-0.
Mycoplasma hyopneumoniae, a component of the porcine respiratory disease complex, colonizes the respiratory tract of swine by binding to the cilia of the bronchial epithelial cells. Mechanisms of pathogenesis are poorly understood for M. hyopneumoniae, but previous work has indicated that it responds to the environmental stressors heat shock, iron deprivation and oxidative compounds. For successful infection, M. hyopneumoniae must effectively resist host responses to the colonization of the respiratory tract. Among these are changes in hormonal levels in the mucosal secretions. Recent work in the stress responses of other bacteria has included the response to the catecholamine norepinephrine. The idea that M. hyopneumoniae can respond to a host hormone, however, is novel and has not previously been demonstrated. To test this, organisms in the early exponential phase of growth were exposed to 100 muM norepinephrine for 4 h, and RNA samples from these cultures were collected and compared to RNA samples from control cultures using two-colour PCR-based M. hyopneumoniae microarrays. The M. hyopneumoniae response included slowed growth and changes in mRNA transcript levels of 84 genes, 53 of which were upregulated in response to norepinephrine. A larger proportion of the genes upregulated than those downregulated were involved with transcription and translation. The downregulated genes were mostly involved with metabolism, which correlated with the reduction in growth of the mycoplasma. Approximately 51 % of the genes were hypothetical with no known function. Thus, in response to norepinephrine, M. hyopneumoniae appears to upregulate protein expression while downregulating general metabolism.
猪肺炎支原体是猪呼吸道疾病综合征的一个组成部分,它通过与支气管上皮细胞的纤毛结合而在猪的呼吸道中定殖。猪肺炎支原体的致病机制尚不清楚,但先前的研究表明,它对热休克、铁缺乏和氧化化合物等环境应激源有反应。为了成功感染,猪肺炎支原体必须有效抵抗宿主对呼吸道定殖的反应。其中包括粘膜分泌物中激素水平的变化。最近关于其他细菌应激反应的研究包括对儿茶酚胺去甲肾上腺素的反应。然而,猪肺炎支原体能够对宿主激素作出反应这一观点是新颖的,以前尚未得到证实。为了验证这一点,将处于生长早期指数期的细菌暴露于100μM去甲肾上腺素中4小时,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将其与对照培养物的RNA样本进行比较。猪肺炎支原体的反应包括生长减缓以及84个基因的mRNA转录水平发生变化,其中53个基因在去甲肾上腺素的作用下上调。上调的基因中,与转录和翻译相关的比例高于下调的基因。下调的基因大多与代谢有关,这与支原体生长的减少相关。大约51%的基因是功能未知的假设基因。因此,对去甲肾上腺素的反应中,猪肺炎支原体似乎上调了蛋白质表达,同时下调了一般代谢。