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Listeria-infected macrophages promote biomechanical alterations in endothelial cell monolayers for transmigration

Marie Muenkel1, Kathryn Wright2, Erva Keskin1

  • 1Interfaculty Institute of Microbiology and Infection Medicine, University of Tübingen, Tübingen, 72076 Baden-Württemberg, Germany; Cluster of Excellence EXC 2124 Controlling Microbes to Fight Infections, University of Tübingen, Tübingen, 72076 Baden-Württemberg, Germany.

Cell Reports
|February 26, 2026
PubMed

Insights

Listeria monocytogenes (LM) infection weakens endothelial cells' barrier function, allowing infected macrophages to spread pathogens. This study reveals how LM manipulates host cells for dissemination.

Area of Science:

  • Cell Biology
  • Pathogen-Host Interactions
  • Biophysics

Background:

  • Intracellular pathogens like Listeria monocytogenes (LM) spread via host cell manipulation.
  • LM hijacks mononuclear phagocytes to cross endothelial cell (EC) barriers, but EC regulation is unclear.

Purpose of the Study:

  • To investigate how LM infection alters endothelial cell (EC) biomechanical responses to macrophages (MΦs).
  • To understand the role of EC biomechanics in LM-infected MΦ transmigration.

Main Methods:

  • Utilized videomicroscopy to observe EC-MΦ interactions.
  • Assessed EC polarization, motility, traction, and monolayer stresses.
  • Examined endothelial permeability and phagocyte extravasation in a zebrafish model.

Main Results:

  • LM infection significantly alters EC biomechanical responses to MΦs.
  • Uninfected MΦs enhance EC barrier integrity, while LM-infected MΦs attenuate this response.
  • Endothelial permeability and phagocyte extravasation increased during LM infection in vivo.

Conclusions:

  • LM infection overrides MΦ-induced endothelial barrier strengthening, promoting pathogen dissemination.
  • This highlights a biomechanical strategy employed by LM for spreading.
  • Findings may inform strategies for infection control.
Keywords:
CP: cell biologyCP: microbiologyListeria monocytogenesbacterial infectioncell adhesioncell biomechanicsendothelial cellshost-pathogen interactionsinfected macrophagetraction force microscopytransmigrationvascular permeabilityzebrafish model

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