Xu Fuzhou, Wu Cun, Guo Fangfang, Cui Guolin, Zeng Ximin, Yang Bing, Lin Jun
Beijing Key Laboratory for Prevention and Control of Infectious Diseases in Livestock and Poultry, Institute of Animal Husbandry and Veterinary Medicine, Beijing Academy of Agriculture and Forestry Sciences Beijing, China.
Department of Animal Science, The University of Tennessee Knoxville, TN, USA.
Front Microbiol. 2015 May 18;6:452. doi: 10.3389/fmicb.2015.00452. eCollection 2015.
Upon colonization in the host gastrointestinal tract, the enteric bacterial pathogen Campylobacter jejuni is exposed to a variety of signaling molecules including the catecholamine hormones epinephrine (Epi) and norepinephrine (NE). NE has been observed to stimulate the growth and potentially enhance the pathogenicity of C. jejuni. However, the underlying mechanisms are still largely unknown. In this study, both Epi and NE were also observed to promote C. jejuni growth in MEMα-based iron-restricted medium. Adhesion and invasion of Caco-2 cells by C. jejuni were also enhanced upon exposure to Epi or NE. To further examine the effect of Epi or NE on the pathobiology of C. jejuni, transcriptomic profiles were conducted for C. jejuni NCTC 11168 that was cultured in iron-restricted medium supplemented with Epi or NE. Compared to the genes expressed in the absence of the catecholamine hormones, 183 and 156 genes were differentially expressed in C. jejuni NCTC 11168 that was grown in the presence of Epi and NE, respectively. Of these differentially expressed genes, 102 genes were common for both Epi and NE treatments. The genes differentially expressed by Epi or NE are involved in diverse cellular functions including iron uptake, motility, virulence, oxidative stress response, nitrosative stress tolerance, enzyme metabolism, DNA repair and metabolism and ribosomal protein biosynthesis. The transcriptome analysis indicated that Epi and NE have similar effects on the gene expression of C. jejuni, and provided insights into the delicate interaction between C. jejuni and intestinal stress hormones in the host.
在肠道细菌病原体空肠弯曲菌定殖于宿主胃肠道后，它会接触到多种信号分子，包括儿茶酚胺激素肾上腺素（Epi）和去甲肾上腺素（NE）。已观察到NE可刺激空肠弯曲菌的生长，并可能增强其致病性。然而，其潜在机制仍 largely 未知。在本研究中，还观察到Epi和NE均可促进空肠弯曲菌在基于MEMα的铁限制培养基中的生长。暴露于Epi或NE后，空肠弯曲菌对Caco-2细胞的黏附和侵袭也增强。为了进一步研究Epi或NE对空肠弯曲菌病理生物学的影响，对在补充有Epi或NE的铁限制培养基中培养的空肠弯曲菌NCTC 11168进行了转录组分析。与在不存在儿茶酚胺激素的情况下表达的基因相比，分别在存在Epi和NE的情况下生长的空肠弯曲菌NCTC 11168中有183个和156个基因差异表达。在这些差异表达的基因中，有102个基因在Epi和NE处理中是共同的。由Epi或NE差异表达的基因涉及多种细胞功能，包括铁摄取、运动性、毒力、氧化应激反应、亚硝化应激耐受性、酶代谢、DNA修复和代谢以及核糖体蛋白生物合成。转录组分析表明，Epi和NE对空肠弯曲菌的基因表达具有相似的影响，并为宿主中空肠弯曲菌与肠道应激激素之间的微妙相互作用提供了见解。
