Development of bioassays using the zebrafish larva model to screen endocrine disruptors for their involvement in the pathological progression of non-alcoholic fatty liver diseases

International audienc

Activated CD4(+) T Cells impact adipose-serived stromal cell function through CD40-dependant activation

International audienc

Temperature-induced liquid crystal microdroplet formation in a partially miscible liquid mixture

Liquid-in-liquid droplets are typically generated by the partitioning of immiscible fluids, e.g. by mechanical shearing with macroscopic homogenisers or microfluidic flow focussing. In contrast, partially miscible liquids with a critical solution temperature display a temperature-dependent mixing behaviour. In this work, we demonstrate how, for a blend of methanol (MeOH) and the thermotropic liquid crystal (LC) 4-Cyano-4 '-pentylbiphenyl (5CB), cooling from a miscible to an immiscible state allows the controlled formation of microdroplets. A near-room-temperature-induced phase separation leads to nucleation, growth and coalescence of mesogen-rich droplets. The size and number of the droplets is tunable on the microscopic scale by variation of temperature quench depth and cooling rate. Further cooling induces a phase transition to nematic droplets with radial configuration, well-defined sizes and stability over the course of an hour. This temperature-induced approach offers a scalable and reversible alternative to droplet formation with relevance in diagnostics, optoelectronics, materials templating and extraction processes

Temperature-Induced Liquid Crystal Microdroplet Formation in a Partially Miscible Liquid Mixture

The controlled formation of microdroplets through temperature variation is an intriguing concept for binary liquid mixtures with a critical solution temperature. Here, we investigate this phenomenon for a blend of methanol (MeOH) and a thermotropic liquid crystal (LC) 4-Cyano-4’-pentylbiphenyl (5CB). A near-room-temperatureinduced phase separation leads to nucleation, growth and coalescence of mesogen-rich droplets. The size and number of the droplets is tunable on the microscopic scale by variation of temperature quench depth and cooling rate. Further cooling induces a phase transition to nematic droplets with radial configuration, well-defined sizes and stability over the course of an hour. This fully reversible process is an interesting material system with relevance in diagnostics, optoelectronics, materials templating and extraction processes.<br /

CD40L-expressing CD4+ T cells prime adipose-derived stromal cells to produce inflammatory chemokines

International audienceThe therapeutic potential of culture-adapted adipose-derived stromal cells (ASCs) is largely related to their production of immunosuppressive factors that are inducible in vitro by priming with inflammatory stimuli, in particular tumor necrosis factor-α (TNFα) and interferon-γ (IFNγ). In vivo, obesity is associated with chronic inflammation of white adipose tissue, including accumulation of neutrophils, infiltration by IFNγ/TNFα-producing immune cells, and ASC dysfunction. In the current study, we identified in obese patients a simultaneous upregulation of CD40Lin the adipose tissue stroma vascular fraction (AT-SVF), correlated with the Th1 gene signature, and an overexpression of CD40 by native ASCs. Moreover, activated CD4+ T cells upregulated CD40 on culture-expanded ASCs and triggered their production of IL-8 in a CD40L-dependent manner, leading to an increased capacity to recruit neutrophils. Finally, activation of ASCs by sCD40L or CD40L-expressing CD4+ T cells relies on both canonical and non-canonical NF-κB pathways, and IL-8 was found to be coregulated with NF-κB family members in AT-SVF. These data identify the CD40-CD40L axis as a priming mechanism of ASCs, able to modulate their cross talk with neutrophils in an inflammatory context, and their functional capacity for therapeutic applications

Comparative immune profiling of acute respiratory distress syndrome patients with or without SARS-CoV2 infection

International audienceAcute respiratory distress syndrome (ARDS) is the main complication of coronavirus disease 2019 (COVID-19), requiring admission to the intensive care unit (ICU). Despite extensive immune profiling of COVID-19 patients, to what extent COVID-19-associated ARDS differs from other causes of ARDS remains unknown. To address this question, here, we build 3 cohorts of patients categorized in COVID-19ARDS, COVID-19ARDS, and COVID-19ARDS, and compare, by high-dimensional mass cytometry, their immune landscape. A cell signature associating S100A9/calprotectin-producing CD169 monocytes, plasmablasts, and Th1 cells is found in COVID-19ARDS, unlike COVID-19ARDS patients. Moreover, this signature is essentially shared with COVID-19ARDS patients, suggesting that severe COVID-19 patients, whether or not they experience ARDS, display similar immune profiles. We show an increase in CD14HLA-DR and CD14CD16 monocytes correlating to the occurrence of adverse events during the ICU stay. We demonstrate that COVID-19-associated ARDS displays a specific immune profile and may benefit from personalized therapy in addition to standard ARDS management