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Fusobacterium nucleatum outer membrane proteins Fap2 and RadD induce cell death in human lymphocytes

Christopher W Kaplan1, Xiaoyuan Ma, Avina Paranjpe

  • 1Molecular Biology Institute, University of California, Los Angeles, California 90095, USA.

Infection and Immunity
|September 9, 2010
PubMed

Insights

Fusobacterium nucleatum induces human lymphocyte cell death using outer membrane proteins Fap2 and RadD. This mechanism bypasses the need for active protein transfer, highlighting a novel bacterial virulence strategy.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Bacterial induction of host cell death is a key virulence factor.
  • Known mechanisms involve bacterial protein transfer via secretion systems.
  • Fusobacterium nucleatum is an oral pathogen implicated in various infections.

Purpose of the Study:

  • To elucidate the mechanism by which Fusobacterium nucleatum induces cell death in human lymphocytes.
  • To identify specific bacterial factors responsible for this cell death induction.

Main Methods:

  • Genetic inactivation of outer membrane proteins (OMPs) Fap2 and RadD in Fusobacterium nucleatum.
  • Cell death assays using human Jurkat T-lymphoma cells.
  • Biochemical and molecular analyses of bacterial membranes.

Main Results:

  • Inactivation of Fap2 and RadD significantly reduced Fusobacterium nucleatum's ability to induce Jurkat cell death.
  • A double mutant lacking both Fap2 and RadD showed almost complete attenuation of cell death induction.
  • Cell-free Fusobacterium nucleatum membranes were sufficient to induce lymphocyte cell death.

Conclusions:

  • Fusobacterium nucleatum utilizes outer membrane proteins Fap2 and RadD to induce human lymphocyte cell death.
  • This mechanism does not require active protein transfer into host cells.
  • Outer membrane proteins alone can mediate bacterial-induced eukaryotic cell death, representing a novel virulence strategy.

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