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Very late antigen-5 and complement receptor type 3 cooperatively mediate the interaction between Bordetella pertussis

W L Hazenbos1, B M van den Berg, R van Furth

  • 1Department of Infectious Diseases, University Hospital Leiden, The Netherlands.

Insights

Very late antigen-5 (VLA-5) on monocytes mediates Bordetella pertussis attachment. Cross-linking VLA-5 enhances complement receptor type 3 (CR3) binding, facilitating bacterial adhesion to monocytes during whooping cough infection.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Bordetella pertussis, the whooping cough pathogen, adheres to and is ingested by human monocytes.
  • Complement receptor type 3 (CR3) on macrophages binds Bordetella pertussis filamentous hemagglutinin.

Purpose of the Study:

  • To investigate the role of very late antigen-5 (VLA-5) in Bordetella pertussis attachment to human monocytes.
  • To elucidate the mechanism by which VLA-5 influences bacterial adhesion.

Main Methods:

  • Monocyte attachment assays using soluble fibronectin and monoclonal antibodies (mAbs) against VLA-5.
  • Cross-linking VLA-5 on monocytes using fibronectin or anti-VLA-5 mAb-coated surfaces.
  • Assessing binding of Bordetella pertussis and C3bi-coated sheep erythrocytes.
  • Investigating the role of CR3 using anti-CR3 mAb and a Bordetella pertussis mutant strain.

Main Results:

  • Soluble fibronectin and anti-VLA-5 mAb inhibited Bordetella pertussis attachment to monocytes.
  • Cross-linking VLA-5 enhanced binding of Bordetella pertussis and C3bi-coated erythrocytes, an effect dependent on filamentous hemagglutinin.
  • Enhanced attachment was inhibited by anti-CR3 mAb, and neutrophils showed reduced binding compared to monocytes.

Conclusions:

  • VLA-5 is crucial for Bordetella pertussis attachment to monocytes.
  • VLA-5 cross-linking augments CR3-mediated binding, facilitating bacterial adhesion.
  • A two-step model is proposed: VLA-5 binding/cross-linking enhances CR3 activity for subsequent bacterial adherence.

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