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首页> 外文期刊>Infection and immunity >Rickettsia rickettsii infection of cultured human endothelial cells induces NF-kappaB activation.
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Rickettsia rickettsii infection of cultured human endothelial cells induces NF-kappaB activation.

机译：立克次体立克次体感染培养的人内皮细胞可诱导NF-κB活化。

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Rickettsia rickettsii, the etiologic agent of Rocky Mountain spotted fever, is an obligate intracellular bacterial organism that infects primarily the vascular endothelial cells (EC). A component of the EC response to infection is transcriptional activation, which may contribute to the thrombotic and inflammatory consequences of disease. In this study, we explore R. rickettsii-induced activation of the nuclear factor-kappaB/Rel (NF-kappaB) family of transcription factors involved in early transcriptional responses to injurious stimuli. Two NF-kappaB species were activated by infection and reacted with a double-stranded oligonucleotide probe corresponding to the kappaB binding domain of the murine kappa light-chain gene enhancer. Gel supershift analysis demonstrated the reactivity of these complexes with antibodies against p65 and p50, and the induced species were tentatively identified as p50-p50 homodimers and p50-p65 heterodimers. Semiquantitative reverse transcription-PCR analysis revealed dramatic increases in the steady-state levels of mRNA coding for the inhibitory subunit of NF-kappaB (IkappaB alpha), transcription of which is enhanced by the binding of NF-kappaB within the IkappaB alpha promoter region. NF-kappaB activation was first detected 1.5 h following infection and was biphasic, with an early peak of activation at approximately 3 h, a return to baseline levels at 14 h, and even higher levels of activation at 24 h. It is likely that NF-kappaB activation requires cellular uptake of R. rickettsii, since treatment of EC with cytochalasin B during infection to block entry inhibited activation by only 70% at 3 h. R. rickettsii-induced activation of NF-kappaB may be an important controlling factor in the transcriptional responses of EC to infection with this obligate intracellular organism.
机译：落基山立克次氏病的病原体立克次氏体是专攻主要感染血管内皮细胞（EC）的专性细胞内细菌生物。 EC对感染的反应的一个组成部分是转录激活，这可能导致疾病的血栓形成和炎症后果。在这项研究中，我们探讨了立克次氏体诱导的参与有害伤害早期转录反应的转录因子核因子-kappaB / Rel（NF-kappaB）家族的激活。通过感染激活了两种NF-kappaB物种，并与对应于鼠kappa轻链基因增强子的kappaB结合域的双链寡核苷酸探针反应。凝胶超位移分析证明了这些复合物与针对p65和p50的抗体的反应性，并且将诱导的物种初步鉴定为p50-p50同二聚体和p50-p65异二聚体。半定量逆转录-PCR分析显示，编码NF-kappaB（IkappaB alpha）抑制性亚基的mRNA稳态水平显着增加，其转录因IK-appaB alpha启动子区域内的NF-kappaB结合而增强。感染后1.5 h首先检测到NF-κB激活，并且是双相的，大约在3 h达到激活的早期峰值，在14 h达到基线水平，甚至在24 h达到更高的激活水平。 NF-κB激活可能需要细胞吸收立克次氏体，因为在感染过程中用细胞松弛素B阻断进入EC的EC在3小时内只能抑制70％的激活。立克次氏体诱导的NF-κB活化可能是EC对这种专性细胞内生物体感染的转录反应中的重要控制因素。

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