Biophysical Society Thematic Meeting | Ascona 2026

Mechanobiology of Infection

Poster Abstracts

16-POS Board 16 DECIPHERING THE MECHANOBIOLOGICAL PROCESSES INVOLVED IN VASCULAR ENDOTHELIAL CELL INFECTION Nadine Oder 1,2 ; Julio César Sánchez-Rendón 1,2 ; Erva Keskin 1,2 ; Effie Bastounis 1,2 ; 1 University of Tübingen, Interfaculty Institute of Cell Biology and Infection Medicine, Cluster of Excellence “Controlling Microbes to Fight Infections (CMFI)”, Tübingen, Germany 2 Humboldt-Universität zu Berlin, Institut für Biologie, AG Mikrobielle Infektionsbiologie, Berlin, Germany Endothelial cells (ECs) line blood vessels, forming a barrier against pathogens, such as bacteria. Crucial to the integrity of this barrier is the action of the cytoskeleton, which generates forces and transmits them through focal adhesions to the extracellular matrix (ECM) and through intercellular junctions to neighbouring ECs. External mechanical stimuli such as varying shear stress (SS) and gradients (SSG) from blood flow, as well as changes in subendothelial stiffness, can alter EC mechanotransduction and thus the endothelial barrier function, but how that may impact intracellular infection dissemination has not been previously explored. In this project, we aim to analyze how ECM stiffness and SSG alter EC biomechanics and thereby influence the intracellular spread of pathogenic bacteria through endothelia. To investigate this, we use the facultative intracellular bacterial pathogen Listeria monocytogenes (L. m.) as a model, and apply controlled SSG to EC in monolayer residing on hydrogels of varying stiffness via a multi-well impinging flow jet device compatible with live-cell imaging. Our data indicate that EC on stiffer matrices or under flow increase their traction and monolayer stresses compared to EC on softer matrices or under static conditions. Interestingly, under these conditions where stresses are elevated cell-to-cell spread of L. m. is reduced which correlates also with decreased bacterial doubling time. Future experiments will address the underlying mechanical and molecular mechanisms that lead to decreased intercellular bacterial spread and replication, for EC subject to flow or residing on increased ECM stiffness .This knowledge will contribute to unraveling novel aspects of host-pathogen interactions, EC mechanobiology and in the future potentially set the foundation for therapeutic interventions targeting EC biomechanical processes.

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