LL-37-dsRNA Complexes Modulate Immune Response via RIG-I in Oral Keratinocytes

Hiroki Kato1,2, Kouji Ohta3, Misaki Akagi1

  • 1Department of Oral and Maxillofacial Surgery, Graduate School of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-Ku, Hiroshima, 734-8553, Japan.

Inflammation
|February 10, 2023
PubMed

Insights

The antimicrobial peptide LL-37 enhances inflammatory responses to nucleic acids in oral cells by interacting with double-stranded RNA and the RIG-I receptor. This interaction may contribute to oral inflammatory diseases.

Area of Science:

  • Immunology
  • Molecular Biology
  • Oral Biology

Background:

  • Nucleic acids act as danger signals (PAMPs/DAMPs), triggering inflammation.
  • LL-37, an antimicrobial peptide, modulates immune responses, but its role in nucleic acid-induced inflammation in oral keratinocytes is unclear.

Discussion:

  • LL-37 enhances CXCL10 expression induced by necrotic cell supernatant (NCS) in oral keratinocytes (RT7), an effect reduced by RNase.
  • LL-37 forms complexes with double-stranded RNA (Poly(I:C)) that amplify CXCL10 expression and activate NF-κB.
  • LL-37 facilitates the cytoplasmic translocation of dsRNA, promoting RIG-I-mediated immune responses.

Key Insights:

  • LL-37 binds to dsRNA and enters the cytoplasm.
  • RIG-I activation is crucial for the inflammatory response mediated by LL-37-dsRNA complexes.
  • LL-37 modulates dsRNA-induced inflammation via RIG-I in oral keratinocytes.

Outlook:

  • LL-37's role in RIG-I-mediated dsRNA responses suggests a potential mechanism in oral inflammatory diseases.
  • Further research could explore therapeutic strategies targeting the LL-37-nucleic acid-RIG-I axis.

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