Salt- and pH-induced swelling of a poly(acrylic acid) brush via quartz crystal microbalance w/dissipation (QCM-D).

We infer the swelling/de-swelling behavior of weakly ionizable poly(acrylic acid) (PAA) brushes of 2-39 kDa molar mass in the presence of KCl concentrations from 0.1-1000 mM, pH = 3, 7, and 9, and grafting densities σ = 0.12-2.15 chains per nm2 using a Quartz Crystal Microbalance with Dissipation (QCM-D), confirming and extending the work of Wu et al. to multiple chain lengths. At pH 7 and 9 (above the pKa ∼ 5), the brush initially swells at low KCl ionic strength (<10 mM) in the "osmotic brush" regime, and de-swells at higher salt concentrations, in the "salted brush" regime, and is relatively unaffected at pH 3, below the pKa, as expected. At pH 7, at low and moderate grafting densities, our results in the high-salt "salted brush" regime (Cs > 10 mM salt) agree with the predicted scaling H ∼ Nσ+1/3Cs-1/3 of brush height H, while in the low-salt "osmotic brush" regime (Cs < 10 mM salt), we find H ∼ Nσ+1/3Cs+0.28-0.38, whose dependence on Cs agrees with scaling theory for this regime, but the dependence on σ strongly disagrees with it. The predicted linearity in the degree of polymerization N is confirmed. The new results partially confirm scaling theory and clarify where improved theories and additional data are needed.

Biofilm formation as a virulence determinant of uropathogenic Escherichia coli Dr+ strains.

Urinary tract infections are the most common health problem affecting millions of people each year. Uropathogenic Escherichia coli (UPEC) strains are the major factor causing lower and upper urinary tract infections. UPEC produce several virulence factors among which are surface exposed adhesive organelldes (pili/fimbriae) responsible for colonization, invasion and amplification within uroepithelial cells. The virulence of the uropathogenic E. coli Dr IH11128 is associated with Dr fimbriae belonging to the Dr family of adhesins (associated with diarrhea and urinary tract infections) and a DraD protein capping the linear fiber at the bacterial cell surface. In this study we revealed that biofilm development can be another urovirulence determinant allowing pathogenic E. coli Dr+ to survive within the urinary tract. E. coli strains were grown in rich or minimal media, allowed to adhere to abiotic surfaces and analyzed microscopically by staining of cells with cristal violet. We found that both Dr fimbriae and DraD, exposed at the cell surface in two forms, fimbria-associated or fimbria non-associated, (DraE+/DraD+, DraE+/DraD- or DraE-/DraD+ E. coli strains) are required for biofilm formation. Additionally, we demonstrated the biofilm formation capacity of E. coli strains deficient in the surface secretion or production of the DraE adhesin.