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首页> 外文期刊>Infection and immunity >Global Gene Expression and the Role of Sigma Factors in Neisseria gonorrhoeae in Interactions with Epithelial Cells
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Global Gene Expression and the Role of Sigma Factors in Neisseria gonorrhoeae in Interactions with Epithelial Cells

机译：淋病奈瑟菌与上皮细胞相互作用的全球基因表达和西格玛因子的作用。

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Like many bacterial pathogens, Neisseria gonorrhoeae must adapt to environmental changes in order to successfully colonize and proliferate in a new host. Modulation of gene expression in response to environmental signals is an efficient mechanism used by bacteria to achieve this goal. Using DNA microarrays and a tissue culture model for gonococcal infection, we examined global changes in gene expression in N. gonorrhoeae in response to adherence to host cells. Among those genes induced upon adherence to human epithelial cells in culture was rpoH, which encodes a homolog of the heat shock sigma factor, σ32 (RpoH), as well as genes of the RpoH regulon, groEL and groES. Attempts to construct an rpoH null mutant in N. gonorrhoeae were unsuccessful, suggesting that RpoH is essential for viability of N. gonorrhoeae. The extracytoplasmic sigma factor, RpoE (σE), while known to regulate rpoH in other bacteria, was found not to be necessary for the up-regulation of rpoH in gonococci upon adherence to host cells. To examine the role of RpoH in host cell interactions, an N. gonorrhoeae strain conditionally expressing rpoH was constructed. The results of our experiments showed that while induction of rpoH expression is not necessary for adherence of gonococci to epithelial cells, it is important for the subsequent invasion step, as gonococci depleted for rpoH invade cells two- to threefold less efficiently than a wild-type strain. Taken together, these results indicate that σ32, but not σE, is important for the response of gonococci in the initial steps of an infection.
机译：像许多细菌性病原体一样，淋病奈瑟氏球菌必须适应环境变化，才能在新宿主中成功定殖和繁殖。响应环境信号而调节基因表达是细菌用于实现该目标的有效机制。使用DNA芯片和用于淋球菌感染的组织培养模型，我们检查了 N基因表达的总体变化。淋病菌对宿主细胞的粘附反应。在粘附于人类上皮细胞培养物中诱导的基因中，有 rpoH ，它编码热休克西格玛因子σ 32 （RpoH）的同源物，以及一些基因。 RpoH调节剂， groEL 和 groES 。尝试在 N中构建一个 rpoH 空突变体。淋球菌未成功，表明RpoH对 N的生存至关重要。淋病菌。已知胞外σ因子RpoE（σ E ）在其他细菌中可以调节 rpoH ，但对于 rpoH的上调并不是必需的附着于宿主细胞后的淋球菌。要检查RpoH在宿主细胞相互作用中的作用，请使用 N。构建了条件表达 rpoH 的淋球菌。我们的实验结果表明，虽然诱导 rpoH 表达对于淋球菌粘附于上皮细胞不是必需的，但对于后续的侵袭步骤却很重要，因为淋巴球菌消耗了 rpoH 入侵细胞的效率比野生型菌株低两倍至三倍。综上所述，这些结果表明，在感染的初始阶段，σ 32 ，而不是σ E ，对淋球菌的反应很重要。

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