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Serratia marcescens serralysin induces inflammatory responses through protease-activated receptor 2

Yutaka Kida1, Hiroyoshi Inoue, Takashi Shimizu

  • 1Department of Bacteriology, Kurume University School of Medicine, 67 Asahi-machi, Kurume, Fukuoka 830-0011, Japan.

Infection and Immunity
|October 18, 2006
PubMed

Insights

Serratia marcescens serralysin activates inflammatory responses by engaging Protease-Activated Receptor 2 (PAR-2). This interaction triggers key transcription factors, AP-1, C/EBPbeta, and NF-kappaB, influencing host immune responses during infection.

Area of Science:

  • Microbiology
  • Immunology
  • Molecular Biology

Background:

  • Serratia marcescens protease serralysin is implicated in infection pathogenesis.
  • Protease-Activated Receptor 2 (PAR-2) mediates inflammatory and immune responses.
  • The role of bacterial proteases, like serralysin, in PAR-2 activation remains unclear.

Purpose of the Study:

  • To investigate if Serratia marcescens serralysin activates host inflammatory responses via PAR-2.
  • To elucidate the molecular mechanisms underlying serralysin-induced inflammation.

Main Methods:

  • Utilized EBC-1 and HeLa cells to study serralysin's effects.
  • Measured interleukin-6 (IL-6) and IL-8 mRNA expression.
  • Assessed activation of AP-1, C/EBP, and NF-kappaB promoters using reporter assays and electrophoretic mobility shift assays.
  • Employed PAR-2 antagonist peptides to confirm the receptor's involvement.

Main Results:

  • Serralysin induced IL-6 and IL-8 mRNA expression in EBC-1 cells.
  • Serralysin activated AP-1, C/EBP, and NF-kappaB transcription factors.
  • Serralysin-induced promoter activation was dependent on PAR-2.
  • PAR-2 antagonist peptides inhibited serralysin-mediated transactivation.

Conclusions:

  • Serralysin activates host inflammatory responses through PAR-2.
  • PAR-2 is crucial for serralysin-induced activation of transcription factors AP-1, C/EBPbeta, and NF-kappaB.
  • This pathway highlights a novel mechanism of bacterial pathogenesis.

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