We investigated the effect of two brush parameters, thickness and dispersity in the molecular weight distribution, on the adhesion of bacteria to pH-responsive poly(acrylic acid) (PAA) brushes synthesized using surface-initiated atom transfer radical polymerization. The attachment and detachment of Staphylococcus epidermidis to PAA brushes at pH 4 and pH 9, respectively, were examined with confocal microscopy. An optimal range of brush thickness, 13-18 nm, was identified for minimizing bacterial adhesion on PAA brushes at pH 4, and bacterial attachment did not depend on the brush dispersity. Increasing either the brush thickness or dispersity detached bacteria from the brushes when the pH was increased from 4 to 9. Bacterial detachment likely arose from an enhanced actuation effect in thick or high-dispersity brushes, as PAA brushes change conformation from collapsed to extended states when the pH is increased from 4 to 9. These results suggest that manipulating the molecular weight distribution provides a route to separately tune the attachment and detachment of bacteria.

We investigate the effect of interfacial properties on the adhesion of bacteria at oil/water interfaces using confocal microscopy. Surfactant-decorated dodecane droplets of diameter 20−60 μm are generated using a coflow microfluidic device, introduced into an aqueous saline suspension of Marinobacter hydrocarbonoclasticus bacteria, and imaged in 3-D over time. Using image analysis algorithms, we determine the number of bacteria adhering at oil/water interfaces over time in the presence of dioctyl sodium succinate (DOSS), a component of the dispersant used in oil-spill recovery. The adsorption of bacteria at the oil/water interface follows Langmuir first-order kinetics for all droplet sizes, with the greatest areal number density of bacteria adhered to the smallest droplets. We vary the surfactant type [DOSS, dicyclohexyl sodium sulfosuccinate, dibutyl sodium sulfosuccinate, cetyltrimethylammonium bromide, and Tween 20] and concentration and examine the effects on long-time adhesion of bacteria. For a fixed droplet size, the areal density of bacteria at the interface decreases with increasing surfactant concentration because of a reduction in oil/water interfacial tension that increases the free energy of adhesion of the bacterium.

Adhesion of bacteria to interfaces is the first step in pathogenic infection, in biofilm formation, and in bioremediation of oil spills and other pollutants. Bacteria use a variety of surface structures to promote interfacial adhesion, with the level of expression of these structures varying in response to local conditions and environmental signals. Here, we investigated how overexpression of type 1 fimbriae, one such appendage, modifies the ability of Escherichia coli to adhere to solid substrates, via biofilm formation and yeast agglomeration, and to oil/water interfaces, via a microbial adhesion to hydrocarbon assay. A plasmid that enables inducible expression of E. coli MG1655 type 1 fimbriae was transformed into fimbriae-deficient mutant strain MG1655ΔfimA. The level of fimH gene expression in the engineered strain, measured using quantitative real-time PCR, could be tuned by changing the concentration of inducer isopropyl β-d-1-thiogalactopyranoside (IPTG), and was higher than that in strain MG1655. Increasing the degree of fimbriation only slightly modified the surface energy and zeta potential of the bacteria, but enhanced their ability to agglomerate yeast cells and to adhere to solid substrates (as measured by biofilm formation) and to oil/water interfaces. We anticipate that the tunable extent of fimbriation accessible with this engineered strain can be used to investigate how adhesin expression modifies the ability of bacteria to adhere to interfaces and to actively self-assemble there.

Adhesion of bacteria to liquid-liquid interfaces can play a role in the biodegradation of dispersed hydrocarbons and in biochemical and bioprocess engineering. Whereas thermodynamic factors underpinning adhesion are well studied,...

Cellular self-digestion is an evolutionarily conserved process occurring in prokaryotic cells that enables survival under stressful conditions by recycling essential energy molecules. Self-digestion, which is triggered by extracellular stress conditions, such as nutrient depletion and overpopulation, induces degradation of intracellular components. This self-inflicted damage renders the bacterium less fit to produce building blocks and resume growth upon exposure to fresh nutrients. However, self-digestion may also provide temporary protection from antibiotics until the self-digestion-mediated damage is repaired. In fact, many persistence mechanisms identified to date may be directly or indirectly related to self-digestion, as these processes are also mediated by many degradative enzymes, including proteases and ribonucleases (RNases). In this review article, we will discuss the potential roles of self-digestion in bacterial persistence.