Department of Preventive Environment and Nutrition, Institute of Biomedical Science, Tokushima University, Tokushima, Japan.
Bacterial and Parasitic Disease Research Division, National Institute of Animal Health, National Agriculture and Food Research Organization, Ibaraki, Japan.
PLoS One. 2018 Oct 15;13(10):e0205865. doi: 10.1371/journal.pone.0205865. eCollection 2018.
Campylobacter jejuni is a major cause of bacterial foodborne illness in humans worldwide. Bacterial entry into a host eukaryotic cell involves the initial steps of adherence and invasion, which generally activate several cell-signaling pathways that induce the activation of innate defense systems, which leads to the release of proinflammatory cytokines and induction of apoptosis. Recent studies have reported that the unfolded protein response (UPR), a system to clear unfolded proteins from the endoplasmic reticulum (ER), also participates in the activation of cellular defense mechanisms in response to bacterial infection. However, no study has yet investigated the role of UPR in C. jejuni infection. Hence, the aim of this study was to deduce the role of UPR signaling via induction of ER stress in the process of C. jejuni infection. The results suggest that C. jejuni infection suppresses global protein translation. Also, 12 h of C. jejuni infection induced activation of the eIF2α pathway and expression of the transcription factor CHOP. Interestingly, bacterial invasion was facilitated by knockdown of UPR-associated signaling factors and treatment with the ER stress inducers, thapsigargin and tunicamycin, decreased the invasive ability of C. jejuni. An investigation into the mechanism of UPR-mediated inhibition of C. jejuni invasion showed that UPR signaling did not affect bacterial adhesion to or survival in the host cells. Further, Salmonella Enteritidis or FITC-dextran intake were not regulated by UPR signaling. These results indicated that the effect of UPR on intracellular intake was specifically found in C. jejuni infection. These findings are the first to describe the role of UPR in C. jejuni infection and revealed the participation of a new signaling pathway in C. jejuni invasion. UPR signaling is involved in defense against the early step of C. jejuni invasion and thus presents a potential therapeutic target for the treatment of C. jejuni infection.
空肠弯曲菌是全球人类细菌性食源性疾病的主要病因。细菌进入宿主真核细胞涉及初始的黏附和入侵步骤,这通常会激活几种细胞信号通路,诱导固有防御系统的激活,导致促炎细胞因子的释放和细胞凋亡的诱导。最近的研究报告称,未折叠蛋白反应(UPR)是从内质网(ER)中清除未折叠蛋白的系统,也参与了细菌感染时细胞防御机制的激活。然而,目前尚无研究探讨 UPR 在空肠弯曲菌感染中的作用。因此,本研究旨在通过诱导 ER 应激推断 UPR 信号在空肠弯曲菌感染过程中的作用。结果表明,空肠弯曲菌感染抑制了全局蛋白翻译。此外,空肠弯曲菌感染 12 小时诱导 eIF2α 通路的激活和转录因子 CHOP 的表达。有趣的是,UPR 相关信号因子的敲低和内质网应激诱导剂(他普西醇和衣霉素)的处理促进了细菌的入侵,降低了空肠弯曲菌的侵袭能力。对 UPR 介导的空肠弯曲菌入侵抑制机制的研究表明,UPR 信号不影响细菌对宿主细胞的黏附和存活。此外,UPR 信号也不调节肠炎沙门氏菌或 FITC-葡聚糖的摄取。这些结果表明,UPR 对细胞内摄取的影响仅在空肠弯曲菌感染中发现。这些发现首次描述了 UPR 在空肠弯曲菌感染中的作用,并揭示了新的信号通路参与空肠弯曲菌的入侵。UPR 信号参与了对空肠弯曲菌早期入侵的防御,因此为空肠弯曲菌感染的治疗提供了一个潜在的治疗靶点。