Background Campylobacter jejuni (C. jejuni) has been assigned as an important food-borne pathogen for human health but many pathogenicity factors of C. jejuni and human host cell responses related to the infection have not yet been adequately clarified. This study aimed to determine further C. jejuni pathogenicity factors and virulence genes based on a random mutagenesis approach. A transposon mutant library of C. jejuni NCTC 11168 was constructed and the ability of individual mutants to adhere to and invade human intestinal epithelial cells was evaluated compared to the wild type. We identified two mutants of C. jejuni possessing altered phenotypes with transposon insertions in the genes Cj1492c and Cj1507c. Cj1492c is annotated as a two-component sensor and Cj1507c is described as a regulatory protein. However, functions of both mutated genes are not clarified so far. Results In comparison to the wild type, Cj::1492c and Cj::1507c showed around 70-80% relative motility and Cj::1492c had around 3-times enhanced adhesion and invasion rates whereas Cj::1507c had significantly impaired adhesive and invasive capability. Moreover, Cj::1492c had a longer lag phase and slower growth rate while Cj::1507c showed similar growth compared to the wild type. Between 5 and 24 h post infection, more than 60% of the intracellular wild type C. jejuni were eliminated in HT-29/B6 cells, however, significantly fewer mutants were able to survive intracellularly. Nevertheless, no difference in host cell viability and induction of the pro-inflammatory chemokine IL-8 were determined between both mutants and the wild type. Conclusion We conclude that genes regulated by Cj1507c have an impact on efficient adhesion, invasion and intracellular survival of C. jejuni in HT-29/B6 cells. Furthermore, potential signal sensing by Cj1492c seems to lead to limiting attachment and hence internalisation of C. jejuni. However, as the intracellular survival capacities are reduced, we suggest that signal sensing by Cj1492c impacts several processes related to pathogenicity of C. jejuni.

中文翻译：

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空肠弯曲杆菌基因 Cj1492c 和 Cj1507c 参与宿主细胞的粘附和侵袭。

背景 空肠弯曲杆菌 (C. jejuni) 已被指定为人类健康的重要食源性病原体，但空肠弯曲杆菌的许多致病因素和与感染相关的人类宿主细胞反应尚未得到充分阐明。本研究旨在基于随机诱变方法进一步确定空肠弯曲菌致病因子和毒力基因。构建了空肠弯曲菌 NCTC 11168 的转座子突变体库，并与野生型相比评估了单个突变体粘附和侵入人肠上皮细胞的能力。我们鉴定了两个空肠弯曲菌突变体，它们具有改变的表型，在基因 Cj1492c 和 Cj1507c 中具有转座子插入。Cj1492c 被注释为双组分传感器，Cj1507c 被描述为调节蛋白。然而，到目前为止，这两个突变基因的功能尚未阐明。结果 与野生型相比，Cj::1492c 和 Cj::1507c 显示出约 70-80% 的相对运动性，Cj::1492c 的粘附和侵袭率提高了约 3 倍，而 Cj::1507c 的粘附和侵袭率明显受损。侵入能力。此外，Cj::1492c 具有较长的滞后期和较慢的生长速度，而 Cj::1507c 与野生型相比表现出相似的生长。在感染后 5 到 24 小时之间，超过 60% 的细胞内野生型空肠弯曲菌在 HT-29/B6 细胞中被消除，然而，能够在细胞内存活的突变体显着减少。然而，在突变体和野生型之间没有确定宿主细胞活力和促炎趋化因子IL-8的诱导差异。结论 我们得出结论，Cj1507c 调控的基因对空肠弯曲杆菌在HT-29/B6 细胞中的有效粘附、侵袭和细胞内存活有影响。此外，Cj1492c 的潜在信号感应似乎导致限制附着，从而限制空肠弯曲菌的内化。然而，随着细胞内存活能力的降低，我们认为 Cj1492c 的信号感应会影响与空肠弯曲菌致病性相关的几个过程。