作者: Carla MT Bauer , Stephanie J DeWitte-Orr , Kyle R Hornby , Caleb CJ Zavitz , Brian D Lichty
关键词: Interferon 、 ISG15 、 Cancer research 、 Fibroblast 、 Immunology 、 STAT1 、 Interferon type I 、 Biology 、 Transcription factor 、 Cell culture 、 Interferon inducer
摘要: The objective of this study was to investigate the impact cigarette smoke on innate antiviral defense mechanisms; specifically, we examined effects induction type I interferon (IFN). We observed a dose-dependent decrease in ability human lung fibroblast and epithelial cells elicit an response against viral double-strand RNA (dsRNA) mimic, polyI:C, presence smoke-conditioned medium (SCM). Mechanistically, SCM decreases expression IFN-stimulated gene 15 (ISG15) IFN regulatory factor-7 (IRF-7) transcripts suppresses nuclear translocation key transcription factors, factor-kappaB (NF-kappaB) IRF-3, after polyI:C stimulation. Furthermore, provide evidence that intercellular strategy infection is also impaired. fibroblasts state IFN-beta This associated with decreased phosphorylated Stat1 treatment. elicited by are reversible almost entirely abrogated antioxidant, such as glutathione. Our findings suggest affects immediate-early, inductive, amplification phases response.