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Actinobacillus actinomycetemcomitans toxin induces both cell cycle arrest in the G2/M phase and apoptosis

M Ohguchi1, A Ishisaki, N Okahashi

  • 1Department of Oral Science, National Institute of Infectious Diseases, Shinjuku-ku, Tokyo 162-8640, Japan.

Infection and Immunity
|November 24, 1998
PubMed

Insights

The bacterium Actinobacillus actinomycetemcomitans produces a toxin that causes B lymphocyte apoptosis and cell cycle arrest, contributing to periodontal disease development. This toxin induces programmed cell death via a Bcl-2-inhibitable pathway.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Periodontopathic bacterium Actinobacillus actinomycetemcomitans is associated with periodontal diseases.
  • The bacterium's culture supernatant exhibits cytotoxic effects on various cell lines.

Purpose of the Study:

  • To purify and characterize the toxin produced by Actinobacillus actinomycetemcomitans.
  • To elucidate the mechanism of cell death induced by the purified toxin in B-cell hybridoma cells.

Main Methods:

  • Toxin purification using a four-step procedure including chromatography.
  • Analysis of protein molecular masses via SDS-PAGE.
  • Assessment of apoptosis using nuclear morphology, DNA fragmentation, and flow cytometry.
  • Investigation of cell cycle effects and the role of Bcl-2 and DNA endonuclease inhibitors.

Main Results:

  • A toxin was purified, yielding two major protein bands at 80 and 85 kDa.
  • The toxin induced apoptosis in HS-72 B-cell hybridoma cells through a Bcl-2-inhibitable mechanism.
  • Flow cytometry revealed G2/M phase cell cycle arrest and apoptosis.
  • A DNA endonuclease inhibitor reduced apoptosis but not cell cycle arrest.

Conclusions:

  • The toxin from Actinobacillus actinomycetemcomitans induces apoptosis and G2/M cell cycle arrest in B lymphocytes.
  • These mechanisms are implicated in the pathogenesis of periodontal diseases.
  • The findings highlight a potential therapeutic target for periodontal disease treatment.

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