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首页> 美国卫生研究院文献>Infection and Immunity >Campylobacter jejuni-Induced Activation of Dendritic Cells Involves Cooperative Signaling through Toll-Like Receptor 4 (TLR4)-MyD88 and TLR4-TRIF Axes
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Campylobacter jejuni-Induced Activation of Dendritic Cells Involves Cooperative Signaling through Toll-Like Receptor 4 (TLR4)-MyD88 and TLR4-TRIF Axes

机译：空肠弯曲杆菌诱导的树突状细胞激活涉及通过Toll样受体4（TLR4）-MyD88和TLR4-TRIF轴的协作信号。

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Campylobacter jejuni is an important cause of human enteritis and has been linked to the development of autoimmune diseases. Recently we showed that infection of murine dendritic cells (DCs) with C. jejuni resulted in DC activation and induction of Campylobacter-specific Th1-effector responses. Toll-like receptor (TLR) signaling through myeloid differentiation factor 88 (MyD88) and/or Toll-interleukin 1 (IL-1) receptor domain-containing adaptor-inducing beta interferon (IFN-β) (TRIF) is critical in inducing immunity against pathogens. In this study, we investigated the role of TLR2, TLR4, MyD88, and TRIF signaling in C. jejuni-induced inflammatory activation of DCs. DC upregulation of major histocompatibility complex class II and costimulatory molecules after C. jejuni challenge was profoundly impaired by TLR2, TLR4, MyD88, and TRIF deficiencies. Similarly, C. jejuni-induced secretion of IL-12, IL-6, and tumor necrosis factor alpha was significantly inhibited in TLR2−/−, TLR4−/−, MyD88−/−, and TRIF−/− DCs compared to that in wild-type DCs; however, the magnitude of inhibition was greater in MyD88−/−, TRIF−/−, and TLR4−/− DCs than in TLR2−/− DCs. Furthermore, C. jejuni induced interferon regulatory factor 3 phosphorylation and IFN-β secretion by DCs in a TLR4-TRIF-dependent fashion, further demonstrating activation of this pathway by C. jejuni. Importantly, TLR2, TLR4, MyD88, and TRIF deficiencies all markedly impaired the Th1-priming ability of C. jejuni-infected DCs. Thus, our results show that cooperative signaling through the TLR4-MyD88 and TLR4-TRIF axes represents a novel mechanism mediating C. jejuni-induced inflammatory responses of DCs. To our knowledge, such a mechanism has not been demonstrated previously for an intact bacterium.
机译：空肠弯曲菌是人肠炎的重要原因，并与自身免疫性疾病的发展有关。最近，我们显示空肠弯曲杆菌感染鼠树突状细胞（DC）会导致DC激活和弯曲杆菌特异性Th1效应子反应的诱导。通过髓样分化因子88（MyD88）和/或包含Toll-白介素1（IL-1）受体域的衔接子诱导β干扰素（IFN-β）（TRIF）的Toll样受体（TLR）信号在诱导免疫中至关重要抵抗病原体。在这项研究中，我们调查了TLR2，TLR4，MyD88和TRIF信号在空肠弯曲杆菌诱导的DC炎症激活中的作用。 TLR2，TLR4，MyD88和TRIF缺陷严重损害了空肠弯曲杆菌攻击后主要组织相容性复合体II类和共刺激分子的DC上调。同样，空肠弯曲杆菌诱导的IL-12，IL-6和肿瘤坏死因子α的分泌在TLR2 -/-，TLR4 -// ， MyD88 -/-和TRIF -/- DC与野生型DC相比；但是，MyD88 -/-，TRIF -/-和TLR4 -/- DC中的抑制幅度要大于TLR2 < sup>-/- DC。此外，空肠弯曲杆菌以TLR4-TRIF依赖性方式诱导DC干扰素调节因子3的磷酸化和IFN-β分泌，进一步证明了空肠弯曲杆菌对该途径的激活。重要的是，TLR2，TLR4，MyD88和TRIF缺陷均明显损害空肠弯曲杆菌感染的DC的Th1启动能力。因此，我们的结果表明，通过TLR4-MyD88和TLR4-TRIF轴的协同信号代表了介导空肠弯曲杆菌诱导的DC炎症反应的新型机制。就我们所知，完整的细菌以前尚未证明过这种机制。

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