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Bacterial fimbriae activate human peripheral blood monocytes utilizing TLR2, CD14 and CD11a/CD18 as cellular

Tomohiko Ogawa1, Yasuyuki Asai, Masahito Hashimoto

  • 1Department of Oral Microbiology, Asahi University School of Dentistry, Gifu, Japan. tomo527@dent.asahi-u.ac.jp

Insights

Porphyromonas gingivalis fimbriae and a synthetic peptide fragment activate human monocytes, triggering inflammatory responses relevant to periodontal disease progression. This involves key signaling pathways and cell surface receptors.

Area of Science:

  • Microbiology
  • Immunology
  • Periodontology

Background:

  • Bacterial fimbriae, including those from Porphyromonas gingivalis, are crucial adherence factors in microbial pathogenesis.
  • Porphyromonas gingivalis is an anaerobic Gram-negative bacterium implicated in periodontal diseases.

Purpose of the Study:

  • To investigate the role of P. gingivalis fimbriae and a specific peptide (ALTTE) in activating human monocytes.
  • To elucidate the molecular mechanisms underlying P. gingivalis-induced inflammation in monocytes.

Main Methods:

  • Treatment of human peripheral blood monocytes with P. gingivalis fimbriae and the synthetic peptide ALTTE.
  • Analysis of IL-6 mRNA expression, cytokine production, p38 MAP kinase phosphorylation, and NF-kappaB activation.
  • Investigation of the involvement of Toll-like receptor 2 (TLR2), CD14, and CD11a/CD18 (LFA-1) in the cellular response.

Main Results:

  • P. gingivalis fimbriae and ALTTE induced IL-6 mRNA expression and cytokine production in human monocytes.
  • Both stimuli led to p38 MAP kinase phosphorylation and NF-kappaB activation.
  • IL-6 production was mediated through TLR2, CD14, and CD11a/CD18 (LFA-1) on monocytes.

Conclusions:

  • P. gingivalis fimbriae and the peptide ALTTE are potent activators of human monocytes, driving inflammatory responses.
  • These findings highlight the potential role of P. gingivalis components in the pathogenesis of periodontal diseases.
  • The study identifies specific molecular pathways and receptors involved in the inflammatory cascade initiated by P. gingivalis.

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