Vibrio vulnificus quorum-sensing molecule cyclo(Phe-Pro) inhibits RIG-I-mediated antiviral innate immunity

Wooseong Lee, Seung Hoon Lee, Minwoo Kim, Jae Su Moon, Geon Woo Kim, Hae Gwang Jung, In Hwang Kim, Ji Eun Oh, Hi Eun Jung, Heung Kyu Lee, Keun Bon Ku, Dae Gyun Ahn, Seong Jun Kim, Kun Soo Kim, Jong-Won Oh

Research output: Contribution to journalArticle

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Abstract

The recognition of pathogen-derived ligands by pattern recognition receptors activates the innate immune response, but the potential interaction of quorum-sensing (QS) signaling molecules with host anti-viral defenses remains largely unknown. Here we show that the Vibrio vulnificus QS molecule cyclo(Phe-Pro) (cFP) inhibits interferon (IFN)-β production by interfering with retinoic-acid-inducible gene-I (RIG-I) activation. Binding of cFP to the RIG-I 2CARD domain induces a conformational change in RIG-I, preventing the TRIM25-mediated ubiquitination to abrogate IFN production. cFP enhances susceptibility to hepatitis C virus (HCV), as well as Sendai and influenza viruses, each known to be sensed by RIG-I but did not affect the melanoma-differentiation-associated gene 5 (MDA5)-recognition of norovirus. Our results reveal an inter-kingdom network between bacteria, viruses and host that dysregulates host innate responses via a microbial quorum-sensing molecule modulating the response to viral infection.

Original languageEnglish
Article number1606
JournalNature communications
Volume9
Issue number1
DOIs
Publication statusPublished - 2018 Dec 1

Fingerprint

Vibrio vulnificus
Quorum Sensing
immunity
Tretinoin
Innate Immunity
genes
Antiviral Agents
Genes
viruses
acids
Molecules
Viruses
interferon
Interferons
molecules
Pattern Recognition Receptors
Norovirus
Sendai virus
Ubiquitination
hepatitis

All Science Journal Classification (ASJC) codes

  • Chemistry(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Physics and Astronomy(all)

Cite this

Lee, Wooseong ; Lee, Seung Hoon ; Kim, Minwoo ; Moon, Jae Su ; Kim, Geon Woo ; Jung, Hae Gwang ; Kim, In Hwang ; Oh, Ji Eun ; Jung, Hi Eun ; Lee, Heung Kyu ; Ku, Keun Bon ; Ahn, Dae Gyun ; Kim, Seong Jun ; Kim, Kun Soo ; Oh, Jong-Won. / Vibrio vulnificus quorum-sensing molecule cyclo(Phe-Pro) inhibits RIG-I-mediated antiviral innate immunity. In: Nature communications. 2018 ; Vol. 9, No. 1.
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abstract = "The recognition of pathogen-derived ligands by pattern recognition receptors activates the innate immune response, but the potential interaction of quorum-sensing (QS) signaling molecules with host anti-viral defenses remains largely unknown. Here we show that the Vibrio vulnificus QS molecule cyclo(Phe-Pro) (cFP) inhibits interferon (IFN)-β production by interfering with retinoic-acid-inducible gene-I (RIG-I) activation. Binding of cFP to the RIG-I 2CARD domain induces a conformational change in RIG-I, preventing the TRIM25-mediated ubiquitination to abrogate IFN production. cFP enhances susceptibility to hepatitis C virus (HCV), as well as Sendai and influenza viruses, each known to be sensed by RIG-I but did not affect the melanoma-differentiation-associated gene 5 (MDA5)-recognition of norovirus. Our results reveal an inter-kingdom network between bacteria, viruses and host that dysregulates host innate responses via a microbial quorum-sensing molecule modulating the response to viral infection.",
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Lee, W, Lee, SH, Kim, M, Moon, JS, Kim, GW, Jung, HG, Kim, IH, Oh, JE, Jung, HE, Lee, HK, Ku, KB, Ahn, DG, Kim, SJ, Kim, KS & Oh, J-W 2018, 'Vibrio vulnificus quorum-sensing molecule cyclo(Phe-Pro) inhibits RIG-I-mediated antiviral innate immunity', Nature communications, vol. 9, no. 1, 1606. https://doi.org/10.1038/s41467-018-04075-1

Vibrio vulnificus quorum-sensing molecule cyclo(Phe-Pro) inhibits RIG-I-mediated antiviral innate immunity. / Lee, Wooseong; Lee, Seung Hoon; Kim, Minwoo; Moon, Jae Su; Kim, Geon Woo; Jung, Hae Gwang; Kim, In Hwang; Oh, Ji Eun; Jung, Hi Eun; Lee, Heung Kyu; Ku, Keun Bon; Ahn, Dae Gyun; Kim, Seong Jun; Kim, Kun Soo; Oh, Jong-Won.

In: Nature communications, Vol. 9, No. 1, 1606, 01.12.2018.

Research output: Contribution to journalArticle

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AU - Lee, Wooseong

AU - Lee, Seung Hoon

AU - Kim, Minwoo

AU - Moon, Jae Su

AU - Kim, Geon Woo

AU - Jung, Hae Gwang

AU - Kim, In Hwang

AU - Oh, Ji Eun

AU - Jung, Hi Eun

AU - Lee, Heung Kyu

AU - Ku, Keun Bon

AU - Ahn, Dae Gyun

AU - Kim, Seong Jun

AU - Kim, Kun Soo

AU - Oh, Jong-Won

PY - 2018/12/1

Y1 - 2018/12/1

N2 - The recognition of pathogen-derived ligands by pattern recognition receptors activates the innate immune response, but the potential interaction of quorum-sensing (QS) signaling molecules with host anti-viral defenses remains largely unknown. Here we show that the Vibrio vulnificus QS molecule cyclo(Phe-Pro) (cFP) inhibits interferon (IFN)-β production by interfering with retinoic-acid-inducible gene-I (RIG-I) activation. Binding of cFP to the RIG-I 2CARD domain induces a conformational change in RIG-I, preventing the TRIM25-mediated ubiquitination to abrogate IFN production. cFP enhances susceptibility to hepatitis C virus (HCV), as well as Sendai and influenza viruses, each known to be sensed by RIG-I but did not affect the melanoma-differentiation-associated gene 5 (MDA5)-recognition of norovirus. Our results reveal an inter-kingdom network between bacteria, viruses and host that dysregulates host innate responses via a microbial quorum-sensing molecule modulating the response to viral infection.

AB - The recognition of pathogen-derived ligands by pattern recognition receptors activates the innate immune response, but the potential interaction of quorum-sensing (QS) signaling molecules with host anti-viral defenses remains largely unknown. Here we show that the Vibrio vulnificus QS molecule cyclo(Phe-Pro) (cFP) inhibits interferon (IFN)-β production by interfering with retinoic-acid-inducible gene-I (RIG-I) activation. Binding of cFP to the RIG-I 2CARD domain induces a conformational change in RIG-I, preventing the TRIM25-mediated ubiquitination to abrogate IFN production. cFP enhances susceptibility to hepatitis C virus (HCV), as well as Sendai and influenza viruses, each known to be sensed by RIG-I but did not affect the melanoma-differentiation-associated gene 5 (MDA5)-recognition of norovirus. Our results reveal an inter-kingdom network between bacteria, viruses and host that dysregulates host innate responses via a microbial quorum-sensing molecule modulating the response to viral infection.

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