ArticleProceedings of the National Academy of Sciences of the United States of America2020
Mechanical adaptation of monocytes in model lung capillary networks.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Chemokine-Receptor Modulation Shapes Neuroinflammatory and Biomechanical Responses in Organotypic Hippocampal Cultures After Oxygen-Glucose Deprivation.ACS chemical neuroscience · 2026Article
- Noninvasive characterization of oocyte deformability in microconstrictions.Science advances · 2025Article
- Controlling colloidal flow through a microfluidic Y-junction.Communications physics · 2025Article
- Deformation under flow and morphological recovery of cancer cells.Lab on a chip · 2024Article
- Article
- Hypertonic treatment of acute respiratory distress syndrome.Frontiers in bioengineering and biotechnology · 2023Article
- Single-cell analysis reveals chemokine-mediated differential regulation of monocyte mechanics.iScience · 2022Article
- Mobilization of CD11bFrontiers in immunology · 2022Article
- Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proper circulation of white blood cells (WBCs) in the pulmonary vascular bed is crucial for an effective immune response. In this branched vascular network, WBCs have to strongly deform to pass through the narrowest capillaries and bifurcations. Although it is known that this process depends on the cell mechanical properties, it is still poorly understood due to the lack of a comprehensive model of cell mechanics and of physiologically relevant experiments. Here, using an in-house microfluidic device mimicking the pulmonary capillary bed, we show that the dynamics of THP1 monocytes evolves along successive capillary-like channels, from a nonstationary slow motion with hops to a fast and smooth efficient one. We used actin cytoskeleton drugs to modify the traffic dynamics. This led us to propose a simple mechanical model that shows that a very finely tuned cortical tension combined with a high cell viscosity governs the fast transit through the network while preserving cell integrity. We finally highlight that the cortical tension controls the steady-state cell velocity via the viscous friction between the cell and the channel walls.
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Registered trials
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