Global Effects of Catecholamines on Actinobacillus pleuropneumoniae Gene Expression
Global Effects of Catecholamines on Actinobacillus pleuropneumoniae Gene Expression
复制标题
儿茶酚胺对胸膜肺炎放线杆菌基因表达的整体影响
DOI：
10.1371/journal.pone.0031121
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发表时间：
2012-02-08
期刊：
影响因子：
3.7
通讯作者：
Zhou, Rui
中科院分区：
文献类型：
--
作者：
Li, Lu;Xu, Zhuofei;Zhou, Rui
细菌可以利用哺乳动物激素来调节在疾病发展中起重要作用的致病过程。胸膜肺炎放线杆菌是一种重要的猪呼吸道病原菌，给养猪业造成了巨大的经济损失。众所周知，压力对A的结果有影响。胸膜肺炎感染为了检验A.胸膜肺炎菌对应激激素儿茶酚胺有反应，比较了肾上腺素（Epi）和去甲肾上腺素（NE）处理后与未处理菌的基因表达谱。芯片结果显示，158和105个基因的差异表达的存在下，Epi和NE，分别。这些基因被分配到各种功能类别，包括许多毒力因子。只有18个基因受到这两种激素的调控。这些基因包括apxIA（ApxI毒素结构基因）、pgaB（参与生物膜形成）、APL_0443（一种自转运粘附素）和编码潜在激素受体的基因，如tyrP 2、ygiY-ygiX（qseC-qseB）操纵子和narQ-narP（参与硝酸盐代谢）。进一步的研究表明，根据apxIA基因表达的变化，Epi增强细胞毒活性，但NE抑制。生物膜的形成不受任何两种激素的影响，尽管pgaB的表达受到影响。NE诱导了与宿主细胞的粘附，但Epi不诱导，表明除了APL_0443之外，激素还影响其他假定的粘附素。本研究揭示了A.胸膜肺炎的基因表达，包括那些编码毒力因子的基因表达，在对两种儿茶酚胺的反应中发生了改变。对A.胸膜肺炎基因表达的两种激素表明，这种病原体可能有多个响应系统的两种儿茶酚胺。
Bacteria can use mammalian hormones to modulate pathogenic processes that play essential roles in disease development. Actinobacillus pleuropneumoniae is an important porcine respiratory pathogen causing great economic losses in the pig industry globally. Stress is known to contribute to the outcome of A. pleuropneumoniae infection. To test whether A. pleuropneumoniae could respond to stress hormone catecholamines, gene expression profiles after epinephrine (Epi) and norepinephrine (NE) treatment were compared with those from untreated bacteria. The microarray results showed that 158 and 105 genes were differentially expressed in the presence of Epi and NE, respectively. These genes were assigned to various functional categories including many virulence factors. Only 18 genes were regulated by both hormones. These genes included apxIA (the ApxI toxin structural gene), pgaB (involved in biofilm formation), APL_0443 (an autotransporter adhesin) and genes encoding potential hormone receptors such as tyrP2, the ygiY-ygiX (qseC-qseB) operon and narQ-narP (involved in nitrate metabolism). Further investigations demonstrated that cytotoxic activity was enhanced by Epi but repressed by NE in accordance with apxIA gene expression changes. Biofilm formation was not affected by either of the two hormones despite pgaB expression being affected. Adhesion to host cells was induced by NE but not by Epi, suggesting that the hormones affect other putative adhesins in addition to APL_0443. This study revealed that A. pleuropneumoniae gene expression, including those encoding virulence factors, was altered in response to both catecholamines. The differential regulation of A. pleuropneumoniae gene expression by the two hormones suggests that this pathogen may have multiple responsive systems for the two catecholamines.