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TMPRSS2 expression in oral mucosal cells induced by transfected double-stranded RNA and IL-1β

Misaki Akagi1, Kouji Ohta2, Miyuki Sakuma1

  • 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.

Journal of Oral Biosciences
|February 18, 2025
PubMed
Abstract

Insights

Oral mucosal cells express Transmembrane serine protease 2 (TMPRSS2), a key factor in viral entry. Interleukin-1β (IL-1β) and viral nucleic acids significantly increase TMPRSS2 expression, promoting infection.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Transmembrane serine protease 2 (TMPRSS2) is crucial for viral entry into host cells, including SARS-CoV-2 and influenza A.
  • Elevated TMPRSS2 expression is a risk factor for viral infection spread.
  • Understanding TMPRSS2 regulation in oral mucosal cells is vital for controlling viral infections.

Purpose of the Study:

  • To investigate TMPRSS2 expression in oral keratinocytes and fibroblasts.
  • To identify factors that induce TMPRSS2 expression in these oral mucosal cells.
  • To elucidate the role of IL-1β and viral nucleic acids in TMPRSS2 induction.

Main Methods:

  • Examined constitutive TMPRSS2 mRNA and protein expression in oral keratinocytes (RT7) and fibroblasts (GT1).
  • Analyzed TMPRSS2 induction following transfection with nucleic acids (dsRNA, dsDNA) and inflammatory cytokines (IL-1β).
  • Investigated the effect of IL-1β on STAT1 activation in relation to dsRNA-induced TMPRSS2 expression.

Main Results:

  • Oral keratinocytes and fibroblasts constitutively express TMPRSS2.
  • Double-stranded RNA (Poly(I:C)) and double-stranded DNA (poly(dA:dT)) increased TMPRSS2 expression.
  • IL-1β significantly upregulated TMPRSS2, especially in combination with Poly(I:C), and enhanced Poly(I:C)-activated STAT1 signaling.

Conclusions:

  • Oral keratinocytes and fibroblasts expressing TMPRSS2 are susceptible to SARS-CoV-2 and influenza A.
  • IL-1β cooperates with viral components to enhance TMPRSS2 expression, facilitating viral invasion in oral mucosa.
  • Targeting TMPRSS2 in oral mucosal cells could be a strategy to prevent viral infections.

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