Biology subjects

Husson, J.

Publications and source records attributed to Husson, J..

4 recordsLinked to original sources

bioRxiv2026

Multiscale oocyst wall mechanics govern coccidian resistance

Coccidian parasites spread through oocysts, environmental transmission stages that must survive harsh conditions yet rupture on cue inside the host to release infectious sporozoites. How the oocyst wall reconciles these opposing demands is unknown. Using single-oocyst microindentation, quantitative imaging and infection assays in Eimeria acervulina and Eimeria tenella, we show that the bilayered wall is functionally partitioned: the chemically fragile outer layer is mechanically dispensable, while the inner layer bears the mechanical load and remains impermeable to macromolecules and limiting osmotic exchange even after the outer layer is stripped. Oocysts behave as pressurised shells that fail preferentially at the anterior pole, a fixed mechanical weak point that channels sporocyst release regardless of where force is applied. Wall structure, autofluorescence, mechanics and infectivity prove dissociable: bleach removes the outer layer without weakening the wall or fully abolishing infectivity, whereas heat weakens the wall and abolishes infectivity while leaving the bilayered structure intact. These findings define a mechanical logic for coccidian oocyst resistance, disinfection and controlled excystation, and identify the inner wall as the critical target for inactivating environmentally transmitted parasites.

microbiology↗

bioRxiv2026

Reprogrammed neutrophils with impaired transit mechanics drive multi-organ capillary stalling after stroke

Beyond the focal brain lesion, stroke causes systemic complications including cardiac failure, pneumonia, renal injury, and sustained immune dysfunction. The source of this multiorgan vulnerability remains unresolved. By imaging over 16,000 vessels of healthy, inflamed and ischemic brains, we identify a circulating neutrophil subpopulation reprogrammed by stroke into a pathological stalling phenotype, occluding capillaries in the brain, heart, kidneys, retina and lungs. Combining transcriptomics, genetic models, integrated microfluidics, cell mechanics assays, and in vivo imaging, we show that this subpopulation exhibits an atypical morphology, increased actin polymerization, and heightened adhesion that impair transit through capillary networks. This phenotype is present in patients with stroke, transmissible by adoptive transfer, and selectively sensitive to inhibition of the Src-family kinase Fgr. Both pharmacological and genetic inactivation of Fgr normalize neutrophil adhesion, reduce capillary stalls, and improve neurological recovery after stroke. These findings identify immune cell transit failure as a systemic driver of post-stroke pathology and a therapeutic target to improve both cerebral and multiorgan outcomes.

neuroscience↗

bioRxiv2025

Stiffening cells with light

Fluorescence microscopy is widely used to observe structures and dynamic processes in living cells and organisms and is often used as if it were purely innocuous to the cells or structures of interest. However, it can lead to phototoxicity, which can affect the cellular behavior and lead to erroneous interpretations of the observations. The major cause of cell damage through phototoxicity is the production of reactive oxygen species (ROS), which can form crosslinks between intracellular molecules, including proteins and nucleic acids. By using profile microindentation and atomic force microscopy, we demonstrate that the excitation of various fluorescent probes leads to a large increase in the stiffness of several cell types within seconds of illumination. The stiffening exhibits a dose-dependent response, where longer exposure times to exciting light are correlated with larger stiffening. This photostiffening effect explains why T cells loaded with the Fluo-4 Calcium probe stop emitting a protrusion within seconds after the excitation light is turned on. We observed photostiffening in different cell types and fluorophores. We showed that repeated cell indentation alone led to cell stiffening as well as excitation with blue or UV light in the absence of a fluoroph ore. However, in the latter case, the stiffening was much smaller than that when the fluorophore was excited. We used both sharp and blunt indenters to show that stiffening occurred not only at the cell cortex level but also deeper in the cell interior and that photostiffening is independent of actin cytoskeleton organization. We correlated the increase in cell stiffness with the production of intracellular reactive oxygen species and reproduced cell stiffening by incubating cells with a ROS inducer, H2O2. The excitation of the photosensitizer Pheophorbide a, which induces a specific type of reactive oxygen species, namely singlet oxygen, also led to cell stiffening. This study reminds the experimentalists that it is crucial to perform controls when using fluorescence. It further allows us to propose exploiting photostiffening as a new method for rapidly quantifying phototoxicity. SignificanceThis study reveals a direct relationship between fluorescence excitation and cell mechanical properties. The generality of th is phenomenon across diverse fluorophores and cell types highlights the importance of controlling phototoxicity in fluorescence experiments, in particular in complex, quantitative cell biology and biophysical experiments, but also reveals an unexpected rol e of intracellular reactive oxygen species production and identifies cell stiffness as a proxy for assessing the efficacy of photodynamic therapy.

biophysics↗

bioRxiv2019

Single-cell immuno-mechanics: rapid viscoelastic changes are a hallmark of early leukocyte activation.

To accomplish their critical task of removing infected cells and fighting pathogens, leukocytes activate by forming specialized interfaces with other cells. Using an innovative micropipette rheometer, we show in three different cell types that when stimulated by microbeads mimicking target cells, leukocytes become up to ten times stiffer and more viscous. These mechanical changes initiate within seconds after contact and evolve rapidly over minutes. Remarkably, leukocyte elastic and viscous properties evolve in parallel, preserving a well-defined ratio that constitutes a mechanical signature specific to each cell type. The current results indicate that simultaneously tracking both elastic and viscous properties during an active cell process provides a new way to investigate cell mechanical processes. Our findings also suggest that dynamic immuno-mechanical measurements provide an identifier of leukocyte type and an indicator of the cells state of activation.

biophysics↗