Mukaida N, Murayama T
Department of Molecular Pharmacology, Cancer Research Institute, Kanazawa University.
Rinsho Byori. 1998 Aug;46(8):821-8.
Evidence is accumulating that interleukin-8 (IL-8), discovered as a potent neutrophil chemotactic factor, plays a crucial role in establishing acute neutrophil-mediated inflammation by exerting various activities against non-leukocytic as well as leukocytic cells. Various types of cells can rapidly produce a large amount of IL-8 upon stimulation with inflammatory stimuli, such as lipopolysaccharide, IL-1, and tumor necrosis factor (TNF). However, IL-8 production is tightly regulated at several levels, particularly at the transcriptional levels to prevent aberrant production. Our previous experiments demonstrated that IL-8 gene transcription requires the cooperative activation of a transcription factor, NF-kappa B, with an additional transcription factor, AP-1 or NF-IL6, depending on types of cells and stimuli. In addition, we recently observed that infection with Helicobacter pylori or cytomegalovirus activated NF-kappa B, therapy inducing IL-8 protein secretion as well as IL-8 gene transcription. Moreover, IL-8, in turn, enhanced cytomegalovirus replication and infectious virion production. Collectively, these results suggest the potential involvement of IL-8 in the pathology of bacterial or viral infection.
越来越多的证据表明，白细胞介素-8（IL-8）最初被发现是一种强大的中性粒细胞趋化因子，它通过对非白细胞和白细胞发挥多种作用，在建立急性中性粒细胞介导的炎症中起关键作用。多种类型的细胞在受到炎症刺激（如脂多糖、IL-1和肿瘤坏死因子（TNF））刺激后，能迅速产生大量的IL-8。然而，IL-8的产生在多个水平受到严格调控，特别是在转录水平，以防止异常产生。我们之前的实验表明，IL-8基因转录需要转录因子NF-κB与另一个转录因子AP-1或NF-IL6协同激活，这取决于细胞类型和刺激因素。此外，我们最近观察到，幽门螺杆菌或巨细胞病毒感染可激活NF-κB，诱导IL-8蛋白分泌以及IL-8基因转录。而且，IL-8反过来又增强了巨细胞病毒的复制和感染性病毒粒子的产生。总体而言，这些结果表明IL-8可能参与了细菌或病毒感染的病理过程。
