Bacterial Colonization of Low‐Wettable Surfaces is Driven by Culture Conditions and Topography

Effect of surface low‐wettability on bacterial colonization has become a prominent subject for the development of antibacterial coatings. However, bacteria's fate on such surfaces immersed in liquid as well as causal factors is poorly understood. This question is addressed by using a range of coatings with increasing hydrophobicity, to superhydrophobic, obtained by an atmospheric plasma polymer method allowing series production. Chemistry, wettability, and topography are thoroughly described, as well as bacterial colonization by in situ live imaging up to 24 h culture time in different liquid media. In the extreme case of superhydrophobic coating, substrates are significantly less colonized in biomolecule‐poor liquids and for short‐term culture only. Complex statistical analysis demonstrates that bacterial colonization on these low‐wettable substrates is predominantly controlled by the culture conditions and only secondary by topographic coating's properties (variation in surface structuration with almost constant mean height). Wettability is less responsible for bacterial colonization reduction in these conditions, but allows the coatings to preserve colonization‐prevention properties in nutritive media when topography is masked by fouling. Even after long‐term culture in rich medium, many large places of the superhydrophobic coating are completely free of bacteria in relation to their capacity to preserve air trapping

Human Immunodeficiency Virus type 1 Endocytic Trafficking Through Macrophage Bridging Conduits Facilitates Spread of Infection

Bridging conduits (BC) sustain communication and homeostasis between distant tethered cells. These are also exploited commonly for direct cell-to-cell transfer of microbial agents. Conduits efficiently spread infection, effectively, at speeds faster than fluid phase exchange while shielding the microbe against otherwise effective humoral immunity. Our laboratory has sought to uncover the mechanism(s) for these events for human immunodeficiency virus type one (HIV-1) infection. Indeed, in our prior works HIV-1 Env and Gag antigen and fluorescent virus tracking were shown sequestered into endoplasmic reticulum-Golgi organelles but the outcomes for spreading viral infection remained poorly defined. Herein, we show that HIV-1 specifically traffics through endocytic compartments contained within BC and directing such macrophage-to-macrophage viral transfers. Following clathrin-dependent viral entry, HIV-1 constituents bypass degradation by differential sorting from early to Rab11+ recycling endosomes and multivesicular bodies. Virus-containing endocytic viral cargoes propelled by myosin II through BC spread to neighboring uninfected cells. Disruption of endosomal motility with cytochalasin D, nocodasole and blebbistatin diminish intercellular viral spread. These data lead us to propose that HIV-1 hijacks macrophage endocytic and cytoskeletal machineries for high-speed cell-to-cell spread

Internalization efficiency of adsorbed particles

Internalization efficiency of adsorbed particle

Developpement d'un revetement visant a ameliorer les proprietes d'etancheite d'un joint elastomere en milieu corrosif

International audienc

Développement d'un revêtement visant à améliorer les propriétés d'étanchéité d'un joint élastomère en milieu corrosif

International audienc

Anti-Reflecting Absorbing Layers for Electrochemical and Biophotonic Applications

International audienc