Role of RIG-I, MDA-5, and PKR on the Expression of Inflammatory Chemokines Induced by Synthetic dsRNA in Airway Epithelial Cells

@article{Matsukura2007RoleOR,
  title={Role of RIG-I, MDA-5, and PKR on the Expression of Inflammatory Chemokines Induced by Synthetic dsRNA in Airway Epithelial Cells},
  author={Satoshi Matsukura and Fumio Kokubu and Masatsugu Kurokawa and Mio Kawaguchi and Koushi Ieki and Hideki Kuga and Miho Odaka and Shintaro Suzuki and Shin Watanabe and Tetsuya Homma and Hiroko T Takeuchi and Kyoko Nohtomi and Mitsuru Adachi},
  journal={International Archives of Allergy and Immunology},
  year={2007},
  volume={143},
  pages={80 - 83}
}
Background: We hypothesized that synthetic double-stranded (ds)RNA may mimic viral infection and reported that dsRNA stimulates expression of inflammatory chemokines through a receptor of dsRNA Toll-like receptor (TLR) 3 in airway epithelial cells. In this study, we focused our study on the role of other receptors for dsRNA, such as retinoic acid-inducible gene I (RIG-I), melanoma differentiation-associated gene 5 (MDA-5), and double-stranded RNA-dependent protein kinase (PKR). Methods: Airway… 
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References

SHOWING 1-10 OF 11 REFERENCES
Expression of IP-10/CXCL10 Is Upregulated by Double-Stranded RNA in BEAS-2B Bronchial Epithelial Cells
TLDR
IP-10 may contribute to antiviral activity through the activation of Th-1-type immunity, and RIG-I and IRF-3 may be involved in this reaction.
Activation of airway epithelial cells by toll-like receptor agonists.
TLDR
The results suggest that airway epithelial cells express several TLRs and that they are functionally active, which may be of importance in inflammation and immunity in the airways in response to inhaled pathogens.
Double-stranded RNA activates RANTES gene transcription through co-operation of nuclear factor-kappaB and interferon regulatory factors in human airway epithelial cells.
  • K. Ieki, S. Matsukura, +9 authors M. Adachi
  • Medicine
    Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
  • 2004
TLDR
Results imply that dsRNA activates NF-kappaB and IRFs and these transcription factors activate transcription of the RANTES promoter and its protein expression in airway epithelial cells.
Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3
TLDR
It is shown that mammalian TLR3 recognizes dsRNA, and that activation of the receptor induces the activation of NF-κB and the production of type I interferons (IFNs).
mda-5: An interferon-inducible putative RNA helicase with double-stranded RNA-dependent ATPase activity and melanoma growth-suppressive properties
Human melanoma cells can be reprogrammed to terminally differentiate and irreversibly lose proliferative capacity by appropriate pharmacological manipulation. Subtraction hybridization identified
Establishment of a monoclonal antibody against human Toll-like receptor 3 that blocks double-stranded RNA-mediated signaling.
TLDR
The mAb against TLR3 reported herein may serve as a regulator for virus-mediated immune response via an alternative pathway involving the dsRNA-TLR3 recognition which might occur on host cells.
The RNA helicase RIG-I has an essential function in double-stranded RNA-induced innate antiviral responses
Intracellular double-stranded RNA (dsRNA) is a chief sign of replication for many viruses. Host mechanisms detect the dsRNA and initiate antiviral responses. In this report, we identify retinoic acid
Corticosteroid and cytokines synergistically enhance toll-like receptor 2 expression in respiratory epithelial cells.
TLDR
Results provide evidence for a novel function of corticosteroids in airway inflammatory disorders, and indicate that the use of inhaled corticosterone in such disorders may have a beneficial role in host defense mechanisms.
Double‐stranded RNA activates RANTES gene transcription through co‐operation of nuclear factor‐κB and interferon regulatory factors in human airway epithelial cells
TLDR
It is hypothesized that dsRNA may mimic viral infection and induce RANTES expression in airway epithelial cells.
Synthetic double‐stranded RNA induces multiple genes related to inflammation through Toll‐like receptor 3 depending on NF‐κB and/or IRF‐3 in airway epithelial cells
  • S. Matsukura, F. Kokubu, +9 authors M. Adachi
  • Biology, Medicine
    Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
  • 2006
Background We hypothesized that synthetic double‐stranded (ds)RNA may mimic viral infection and induce expression of genes related to inflammation in airway epithelial cells.
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