Enhancement of Cell Adhesion by Anaplasma phagocytophilum Nucleolin-Interacting Protein AFAP

Hongcheng Tang1, Daxiu Zhang2, Fenfen Jiang3

  • 1Department of Microbiology, School of Biology & Basic Medical Sciences, Soochow University, Suzhou 215123, China.

Insights

Anaplasma phagocytophilum enhances neutrophil adhesion via AFAP protein. This bacterial protein interacts with host nucleolin, a key factor in promoting cell adhesion during infection.

Area of Science:

  • Microbiology
  • Cell Biology
  • Pathogenesis

Background:

  • Anaplasma phagocytophilum causes human granulocytic anaplasmosis (HGA).
  • The bacterium enhances neutrophil adhesion to endothelial cells during infection.
  • Bacterial factors responsible for this adhesion enhancement are largely unknown.

Purpose of the Study:

  • To characterize the Anaplasma phagocytophilum protein AFAP (actin filament-associated protein).
  • To investigate AFAP's role in enhancing host cell adhesion.
  • To identify host factors interacting with AFAP.

Main Methods:

  • Characterization of AFAP's subcellular localization and dynamics.
  • Tandem affinity purification and mass spectrometry to identify interacting proteins.
  • RNA interference and DNA aptamer treatment to assess nucleolin's role.

Main Results:

  • AFAP dynamically changed its pattern and location within host cells.
  • AFAP was found to enhance endothelial cell adhesion.
  • Host nucleolin was identified as an AFAP-interacting protein.
  • Disruption of nucleolin attenuated AFAP-mediated cell adhesion.

Conclusions:

  • AFAP enhances cell adhesion in a nucleolin-dependent manner.
  • AFAP is a novel bacterial factor contributing to Anaplasma phagocytophilum-mediated cell adhesion.
  • Understanding AFAP-nucleolin interaction advances knowledge of HGA pathogenesis.

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