Biophysical Society Thematic Meeting | Ascona 2026

Mechanobiology of Infection

Poster Abstracts

4-POS Board 4 MENINGOCOCCAL ADHESION ALTERS ENDOTHELIAL CELL CONTRACTILITY VIA A NOVEL STRUCTURE LINKING APICAL INFECTION SISTES TO BASAL ACTIN STRESS FIBERS Gautham Sankara 1 ; Sylvie Goussard 1 ; Guillaume Duménil 1 ; Daria Bonazzi 1,2 ; 1 Institut Pasteur, Paris, France 2 Institut Jacques Monod - CNRS UPC INSERM, Paris, France Ancreopodia are novel actin-rich columnar structures linking apical cortical plaques—induced by Neisseria meningitidis (Nm) adhesion—to basal stress fibers in endothelial cells. This study characterizes Ancreopodia and explores their roles in pathogen-induced mechanotransduction and vascular damage. Using super-resolution microscopy, we identified distinct apical, middle, and basal domains of Ancreopodia, which significantly reorganize basal actin stress fibers, induce focal adhesions, and elevate local traction forces. Dynamic imaging showed synchronized movements between bacterial colonies and basal mechanosensitive proteins (paxillin, vinculin, and non-muscle myosin-II), indicating direct mechanotransduction from apical infection sites to the basal extracellular matrix (ECM). Crucially, Ancreopodia impact cell motility and ECM remodeling, potentially contributing to increase of barrier permeability and vascular damage. Future studies will focus on apico-basal mechanotransduction at the multicellular scale, extending our understanding of Nm pathogenicity and force balance mechanisms involved in breaching of tissue barriers.

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