[Molecular mechanism of interleukin-8 gene expression].
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.
Department of Molecular Pharmacology, Cancer Research Institute, Kanazawa University.
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Mukaida
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T
Murayama
D003587:Cytomegalovirus / Q000502:physiology; D003586:Cytomegalovirus Infections / Q000209:etiology; D005786:Gene Expression Regulation; D016481:Helicobacter Infections / Q000209:etiology; D016480:Helicobacter pylori / Q000502:physiology; D006801:Humans; D016209:Interleukin-8 / Q000235:genetics* / Q000502:physiology; D016328:NF-kappa B / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism; D014158:Transcription, Genetic; D014779:Virus Replication
D016209:Interleukin-8; D016328:NF-kappa B; D014157:Transcription Factors