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Leptospira interrogans, a widespread zoonotic disease, attaches to host cells via vascular endothelial (VE)-cadherin. This interaction facilitates bacterial spread and may cause vascular damage, contributing to leptospirosis symptoms.

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Area of Science:

  • Microbiology
  • Pathogen-host interactions
  • Cell biology

Background:

  • Leptospirosis is a significant global zoonotic disease.
  • Pathogenic Leptospira adhesion to host cells is crucial for infection progression.
  • Previous studies indicated Leptospira binds host cells more than extracellular matrix.

Purpose of the Study:

  • To identify mammalian cell surface receptors for pathogenic Leptospira interrogans.
  • To investigate the role of vascular endothelial (VE)-cadherin in Leptospira adherence to endothelial cells.
  • To understand the implications of this interaction in leptospirosis pathogenesis.

Main Methods:

  • Utilized mass spectrometry and protein arrays to screen for Leptospira receptors.
  • Employed endothelial cell cultures (EA.hy926, HMEC-1) to study bacterial-cell interactions.
  • Performed binding assays with purified VE-cadherin and function-blocking antibodies.

Main Results:

  • Identified cadherin family members, specifically VE-cadherin, as potential receptors for L. interrogans.
  • Demonstrated dose-dependent and saturable binding of L. interrogans to VE-cadherin.
  • Showed that blocking VE-cadherin function significantly reduced bacterial attachment to endothelial cells.
  • Observed disruption of endothelial cell monolayers upon incubation with L. interrogans.

Conclusions:

  • VE-cadherin is a novel mammalian cell surface receptor for L. interrogans.
  • Leptospira attachment to VE-cadherin on endothelial cells contributes to vascular damage.
  • This interaction may facilitate pathogen dissemination and hemorrhagic manifestations in leptospirosis.