Preventing protein adsorption from a range of surfaces using an aqueous fish protein extract

We utilize an aqueous extract of fish proteins (FPs) as a coating for minimizing the adsorption of fibrinogen (Fg) and human serum albumin (HSA). The surfaces include stainless steel (SS), gold (Au), silicon dioxide (SiO 2), and poly(styrene) (PS). The adsorption processes (kinetics and adsorbed mass) are followed by quartz crystal microbalance with dissipation (QCM-D). Complementary surface information is provided by X-ray photoelectron spectroscopy (XPS) and atomic force microscopy (AFM). QCM-D shows no mass increases to any of the FPcoated surfaces upon treating with Fg or HSA. Also, when Fg- or HSA-coated surfaces are exposed to the FPs, a significant increase in adsorbed mass occurs because the FPs are highly surface-active displacing Fg. Additionally, fluorescence microscopy confirms that very little Fg adsorbs to the FP-coated surfaces. We propose that FP coatings prevent protein adsorption by steric stabilization and could be an alternative method for preventing unwanted bioadhesion on medical materials

Microbiotas from UC patients display altered metabolism and reduced ability of LAB to colonize mucus

We compared fecal microbial communities derived either from Ulcerative Colitis (UC) patients in remission (n = 4) or in relapse (n = 4), or from healthy subjects (n = 4). These communities were used for inoculation of a dynamic in vitro gut model, which contained integrated mucin-covered microcosms. We found that the microbiota of the ‘mucus’ largely differed from that of the ‘lumen’. This was partly due to decreased mucus-associated populations of lactic acid producing bacterial populations (LAB), as LAB originating from UC patients had a significantly decreased capacity to colonize the mucin-covered microcosms as compared to those originating from healthy subjects. We found significant differences between the metabolomes of UC patients in relapse and remission, respectively, while the metabolome of patients in remission resembled that of healthy subjects. These novel findings constitute an important contribution to the understanding of the complex etiology of UC