Knut Drescher

Turbulence is ubiquitous, from oceanic currents to small-scale biological and quantum systems. Self-sustained turbulent motion in microbial suspensions presents an intriguing example of collective dynamical behavior among the simplest forms of life and is important for fluid mixing and molecular transport on the microscale. The mathematical characterization of turbulence phenomena in active nonequilibrium fluids proves even more difficult than for conventional liquids or gases. It is not known which features of turbulent phases in living matter are universal or system-specific or which generalizations of the Navier-Stokes equations are able to describe them adequately. Here, we combine experiments, particle simulations, and continuum theory to identify the statistical properties of self-sustained meso-scale turbulence in active systems. To study how dimensionality and boundary conditions affect collective bacterial dynamics, we measured energy spectra and structure functions in dense Bacillus subtilis suspensions in quasi-2D and 3D geometries. Our experimental results for the bacterial flow statistics agree well with predictions from a minimal model for self-propelled rods, suggesting that at high concentrations the collective motion of the bacteria is dominated by short-range interactions. To provide a basis for future theoretical studies, we propose a minimal continuum model for incompressible bacterial flow. A detailed numerical analysis of the 2D case shows that this theory can reproduce many of the experimentally observed features of self-sustained active turbulence.

Bacterial processes ranging from gene expression to motility and biofilm formation are constantly challenged by internal and external noise. While the importance of stochastic fluctuations has been appreciated for chemotaxis, it is currently believed that deterministic long-range fluid dynamical effects govern cell-cell and cell-surface scattering-the elementary events that lead to swarming and collective swimming in active suspensions and to the formation of biofilms. Here, we report direct measurements of the bacterial flow field generated by individual swimming Escherichia coli both far from and near to a solid surface. These experiments allowed us to examine the relative importance of fluid dynamics and rotational diffusion for bacteria. For cell-cell interactions it is shown that thermal and intrinsic stochasticity drown the effects of long-range fluid dynamics, implying that physical interactions between bacteria are determined by steric collisions and near-field lubrication forces. This dominance of short-range forces closely links collective motion in bacterial suspensions to self-organization in driven granular systems, assemblages of biofilaments, and animal flocks. For the scattering of bacteria with surfaces, long-range fluid dynamical interactions are also shown to be negligible before collisions; however, once the bacterium swims along the surface within a few microns after an aligning collision, hydrodynamic effects can contribute to the experimentally observed, long residence times. Because these results are based on purely mechanical properties, they apply to a wide range of microorganisms.

Quorum sensing is a chemical communication process that bacteria use to regulate collective behaviors. Disabling quorum-sensing circuits with small molecules has been proposed as a potential strategy to prevent bacterial pathogenicity. The human pathogen Pseudomonas aeruginosa uses quorum sensing to control virulence and biofilm formation. Here, we analyze synthetic molecules for inhibition of the two P. aeruginosa quorum-sensing receptors, LasR and RhlR. Our most effective compound, meta-bromo-thiolactone (mBTL), inhibits both the production of the virulence factor pyocyanin and biofilm formation. mBTL also protects Caenorhabditis elegans and human lung epithelial cells from killing by P. aeruginosa. Both LasR and RhlR are partially inhibited by mBTL in vivo and in vitro; however, RhlR, not LasR, is the relevant in vivo target. More potent antagonists do not exhibit superior function in impeding virulence. Because LasR and RhlR reciprocally control crucial virulence factors, appropriately tuning rather than completely inhibiting their activities appears to hold the key to blocking pathogenesis in vivo.