Phase separation and rotor self-assembly in active particle suspensions

Adding a non-adsorbing polymer to passive colloids induces an attraction between the particles via the `depletion' mechanism. High enough polymer concentrations lead to phase separation. We combine experiments, theory and simulations to demonstrate that using active colloids (such as motile bacteria) dramatically changes the physics of such mixtures. First, significantly stronger inter-particle attraction is needed to cause phase separation. Secondly, the finite size aggregates formed at lower inter-particle attraction show unidirectional rotation. These micro-rotors demonstrate the self assembly of functional structures using active particles. The angular speed of the rotating clusters scales approximately as the inverse of their size, which may be understood theoretically by assuming that the torques exerted by the outermost bacteria in a cluster add up randomly. Our simulations suggest that both the suppression of phase separation and the self assembly of rotors are generic features of aggregating swimmers, and should therefore occur in a variety of biological and synthetic active particle systems.Comment: Main text: 6 pages, 5 figures. Supplementary information: 5 pages, 4 figures. Supplementary movies available from httP://www.pnas.org/lookup/suppl/doi:10.1073/pnas.1116334109/-/DCSupplementa

Enhanced gas-liquid mass transfer of an oscillatory constricted-tubular reactor

The mass transfer performance has been tested for gas-liquid flow in a new tubular reactor system, the oscillating mesotube (OMT), which features the oscillatory movement of fluid across a series of smooth constrictions located periodically along the vertical 4.4 mm internal diameter tube. The effect of the fluid oscillations (frequency,f, and center-to-peak amplitude, x(0), in the range of 0-20 s(-1) and 0-3 mm, respectively) on the overall volumetric mass transfer coefficient (k(L)a) has been tested by measuring the oxygen saturation levels with a fiber-optical microprobe (oxygen micro-optrode), and a mathematical model has been produced to describe the oxygen mass transport in the OMT. The oxygen mass transfer rates were about I order of magnitude higher (k(L)a values up to 0.16 s(-1)) than those values reported for gas-liquid contacting in a 50 mm internal diameter oscillatory flow reactor (OFR), for the same peak fluid oscillatory velocity, i.e., 2 pi fx(0). This represents remarkable oxygen transfer efficiencies, especially when considering the very low mean superficial gas velocity involved in this work (0.37 mm s(-1)). The narrower constrictions helped to increase the gas fraction (holdup) by reducing the rise velocity of the bubbles. However, the extent of radial mixing and the detachment of vortex rings from the surface of the periodic constrictions are actually the main causes of bubbles retention and effective gas-liquid contacting and are, thus, responsible for the enhancement of k(L)a in the OMT.N.R. thanks the Portuguese Foundation for Science and Technology (FCT) for financial support of his work (SFRH/BD/6954/2001)

Differential Dynamic Microscopy of Bacterial Motility

We demonstrate 'differential dynamic microscopy' (DDM) for the fast, high throughput characterization of the dynamics of active particles. Specifically, we characterize the swimming speed distribution and the fraction of motile cells in suspensions of Escherichia coli bacteria. By averaging over ~10^4 cells, our results are highly accurate compared to conventional tracking. The diffusivity of non-motile cells is enhanced by an amount proportional to the concentration of motile cells.Comment: 4 pages, 4 figures. In this updated version we have added simulations to support our interpretation, and changed the model for the swimming speed probability distribution from log-normal to a Schulz distribution. Neither modification significantly changes our conclusion

Oscillatory surface rheotaxis of swimming E. coli bacteria

Bacterial contamination of biological conducts, catheters or water resources is a major threat to public health and can be amplified by the ability of bacteria to swim upstream. The mechanisms of this rheotaxis, the reorientation with respect to flow gradients, often in complex and confined environments, are still poorly understood. Here, we follow individual E. coli bacteria swimming at surfaces under shear flow with two complementary experimental assays, based on 3D Lagrangian tracking and fluorescent flagellar labelling and we develop a theoretical model for their rheotactic motion. Three transitions are identified with increasing shear rate: Above a first critical shear rate, bacteria shift to swimming upstream. After a second threshold, we report the discovery of an oscillatory rheotaxis. Beyond a third transition, we further observe coexistence of rheotaxis along the positive and negative vorticity directions. A full theoretical analysis explains these regimes and predicts the corresponding critical shear rates. The predicted transitions as well as the oscillation dynamics are in good agreement with experimental observations. Our results shed new light on bacterial transport and reveal new strategies for contamination prevention.Comment: 12 pages, 5 figure

The Role of the Mucus Barrier in Digestion

Mucus forms a protective layer across a variety of epithelial surfaces. In the gastrointestinal (GI) tract, the barrier has to permit the uptake of nutrients, while excluding potential hazards, such as pathogenic bacteria. In this short review article, we look at recent literature on the structure, location, and properties of the mammalian intestinal secreted mucins and the mucus layer they form over a wide range of length scales. In particular, we look at the structure of the gel-forming glycoprotein MUC2, the primary intestinal secreted mucin, and the influence this has on the properties of the mucus layer. We show that, even at the level of the protein backbone, MUC2 is highly heterogeneous and that this is reflected in the networks it forms. It is evident that a combination of charge and pore size determines what can diffuse through the layer to the underlying gut epithelium. This information is important for the targeted delivery of bioactive molecules, including nutrients and pharmaceuticals, and for understanding how GI health is maintained

The interaction of bacterial pathogens with platelets.

In recent years, the frequency of serious cardiovascular infections such as endocarditis has increased, particularly in association with nosocomially acquired antibiotic-resistant pathogens. Growing evidence suggests a crucial role for the interaction of bacteria with human platelets in the pathogenesis of cardiovascular infections. Here, we review the nature of the interactions between platelets and bacteria, and the role of these interactions in the pathogenesis of endocarditis and other cardiovascular diseases

ISG15-dependent stabilisation of USP18 is necessary but not sufficient to regulate type I interferon signalling in humans

Funding: This work was supported by grants from the Academy of Medical Sciences (SBF003/1028 to DJH), Wellcome Trust Institutional Strategic Support Fund (to DJH), Wellcome Trust (101788/Z/13/Z to RER), the UK Medical Research Council (MC_UU_12014/1 to JM and CGGB) and by the Wellcome Trust via a Senior Clinical Research Fellowship (108070/Z/15/Z to MPW). The UK Medical Research Council (MC_UU_00038/8 to KNS). KNS is a Lister Institute Prize Fellow.Type I interferon (IFN) signalling induces the expression of several hundred IFN-stimulated genes (ISGs) that provide an unfavourable environment for viral replication. To prevent an overexuberant response and autoinflammatory disease, IFN signalling requires tight control. One critical regulator is the ubiquitin-like protein IFN-stimulated gene 15 (ISG15), evidenced by autoinflammatory disease in patients with inherited ISG15 deficiencies. Current models suggest that ISG15 stabilises ubiquitin-specific peptidase 18 (USP18), a well-established negative regulator of IFN signalling. USP18 also functions as an ISG15-specific peptidase that cleaves ISG15 from ISGylated proteins; however, USP18's catalytic activity is dispensable for controlling IFN signalling. Here, we show that the ISG15-dependent stabilisation of USP18 involves hydrophobic interactions reliant on tryptophan 123 (W123) in ISG15. Nonetheless, while USP18 stabilisation is necessary, it is not sufficient for the regulation of IFN signalling; ISG15 C-terminal mutants with significantly reduced affinity still stabilised USP18, yet the magnitude of signalling resembled ISG15-deficient cells. Hence, USP18 requires non-covalent interactions with the ISG15 C-terminal diGlycine motif to promote its regulatory function. It shows ISG15 is a repressor of type I IFN signalling beyond its role as a USP18 stabiliser.Peer reviewe