title: Expression of transcription factor genes after influenza A virus infection.
abstract: Infection of human monocytes with influenza A virus induces a broad range of proinflammatory cytokines and mononuclear cell attracting chemokines before the infected cells undergo apoptosis. The underlying mechanisms by which the corresponding genes are transcriptionally initiated after virus infection are still poorly understood. Activation of NF-kappa B seems to play an important role in the regulation of many proinflammatory cytokine genes, but cannot be the only mechanism, since several cytokine genes lack respective binding sites in their promoter regions. Therefore, we additionally investigated other transcription factors of possible importance such as CREB, CTF, OTF-1, and OTF-2. To explore long-term regulatory mechanisms, we investigated the induction of transcription factors on the gene expression level which may be important to substitute for metabolized transcription factor proteins after their activation. We identified a cell-type-specific differential response: CREB, CTF, OTF-1, OFT-2, and NF-kappa B genes were strongly induced 1 to 4 hours after influenza A virus infection in the monocytic cell line Mono Mac 6, while in freshly prepared human monocytes no significant changes were detected. In infected monocytes, which die by apoptosis, the expression of CREB, CTF, and OTF-2 was rather suppressed 8 hours after infection. In conclusion, the long-term regulation of transcription factor gene expression in non-proliferating cells seems to be of minor importance after influenza infection since in apoptosisprone cells an immediate availability of transcription factor proteins is required.
authors.affiliation: Institute of Immunology, Philipps-University Marburg, Marburg, Germany.
authors.forename: D
authors.initials: D
authors.lastname: Bussfeld
authors.forename: M
authors.initials: M
authors.lastname: Bacher
authors.forename: A
authors.initials: A
authors.lastname: Moritz
authors.forename: D
authors.initials: D
authors.lastname: Gemsa
authors.forename: H
authors.initials: H
authors.lastname: Sprenger
mesh_terms: D000818:Animals; D022762:CCAAT-Enhancer-Binding Proteins; D002460:Cell Line; D002478:Cells, Cultured; D017362:Cyclic AMP Response Element-Binding Protein / Q000096:biosynthesis / Q000235:genetics; D004268:DNA-Binding Proteins / Q000096:biosynthesis / Q000235:genetics; D004285:Dogs; D015870:Gene Expression; D051863:Host Cell Factor C1; D006801:Humans; D009980:Influenza A virus / Q000502:physiology*; D009000:Monocytes / Q000166:cytology / Q000378:metabolism / Q000821:virology; D016328:NF-kappa B / Q000096:biosynthesis / Q000235:genetics; D051839:NFI Transcription Factors; D050811:Octamer Transcription Factor-1; D050813:Octamer Transcription Factor-2; D014157:Transcription Factors / Q000096:biosynthesis / Q000235:genetics*
chemical_list: D022762:CCAAT-Enhancer-Binding Proteins; C077305:CTF-1 transcription factor; D017362:Cyclic AMP Response Element-Binding Protein; D004268:DNA-Binding Proteins; C497692:HCFC1 protein, human; D051863:Host Cell Factor C1; D016328:NF-kappa B; D051839:NFI Transcription Factors; D050811:Octamer Transcription Factor-1; D050813:Octamer Transcription Factor-2; C494165:POU2F1 protein, human; C058435:POU2F2 protein, human; D014157:Transcription Factors