Forced desorption of nanoparticles from an oil-water interface.

While nanoparticle adsorption to fluid interfaces has been studied from a fundamental standpoint and exploited in application, the reverse process, that is, desorption and disassembly, remains relatively unexplored. Here we demonstrate the forced desorption of gold nanoparticles capped with amphiphilic ligands from an oil-water interface. A monolayer of nanoparticles is allowed to spontaneously form by adsorption from an aqueous suspension onto a drop of oil and is subsequently compressed by decreasing the drop volume. The surface pressure is monitored by pendant drop tensiometry throughout the process. Upon compression, the nanoparticles are mechanically forced out of the interface into the aqueous phase. An optical method is developed to measure the nanoparticle area density in situ. We show that desorption occurs at a coverage that corresponds to close packing of the ligand-capped particles, suggesting that ligand-induced repulsion plays a crucial role in this process. © 2011 American Chemical Society

Oriented Assembly of Anisotropic Particles by Capillary Interactions

Particles situated at fluid interfaces occur in nature, with the particles ranging from pollen to insects which walk on water. Particles at interfaces are exploited in classical applications like Pickering emulsions, in which particles stabilize emulsions, and froth flotation, in which ore particle adsorption to fluid interfaces is used to separate and recover metal ores. Particles at interfaces also occur in emerging applications in which nanomaterials are organized at interfaces. The assembly of particles into ordered structures via capillary interactions is studied. Early work in this field focused primarily on spherical particles that distort fluid interfaces and create excess area. The particles assembled by capillary interactions which occur because the excess area created by the particles decreases as the particles approach each other. Here, particles with shape anisotropy are studied. Such particles create undulations with excess area that can be locally elevated at certain locations around the particle. The local elevation of excess area makes these sites locations for preferred assembly. Hence, particles orient and aggregate in preferred orientations. Such self assembly is often termed directed assembly. Three key issues in directed assembly are means of controlling the object orientation, alignment, and the sites for preferred assembly, including means of promoting registry of features on particles. Each of these issues is addressed in detail in for the example of a right circular cylinder using analysis, experiment and numerics. A series of other shapes are then studied to illustrate the generality of the concepts developed

HISTONE DEACETYLASES IN INFLAMMATORY BOWEL DISEASES - INFLUENCE ON THE ANTIMICROBIAL BARRIER

The development and clinical behavior of the two major inflammatory bowel diseases (IBD) subgroups Crohn’s disease (CD) and ulcerative colitis (UC), are determined by multiple underlying factors leading to an impaired antimicrobial barrier and chronic inflammation. Contributing environmental influences on the onset of the diseases such as the intestinal microbiota, antibiotics use, smoking, or nutrition have more and more entered the limelight of the field. The increasing incidence of IBD, the big variance in disease progression, and the discrepancy between monocygotic twins urgently impose the question how exactly environmental factors might impact on IBD risk and progression. The emerging field of epigenetics offers a mechanistic framework to dissect the present interplay between environment and genome in the context of IBD and will allow a better understanding of disease pathology. Histone deacetylases (HDACs) are important epigenetic factors implicated in intestinal tissue homeostasis. They deacetylate histones but also a vast number of non-histone proteins, e.g. the transcription factor NF-κB, thereby impacting on transcriptional regulation on different levels. A role for HDACs in the epigenetically-mediated modulation of hBDs has been demonstrated in a number of studies, underscoring a potential involvement of HDACs in the β-defensin-related defects found in colonic IBD. In addition, inhibiting HDACs has been proposed as an IBD intervention, making more detailed studies on the role of HDACs in gut antimicrobial barrier function indespensible. Firstly, in this work, a systematic overview of class I HDAC mRNA intestinal expression has been performed in a large cohort of IBD patients. First insights on the expression pattern on the protein level are also given. Secondly, this study aimed to contribute to the small body of knowledge on HDAC-mediated epigenetic control of antimicrobial peptide (AMP) expression; focusing on human β-defensin 2 (hBD2). Herein, emphasis has been laid on the therapeutically relevant probiotic E. coli Nissle 1917 (EcN) as a potent hBD2-inducing factor in addition to the pro-inflammatory cytokine IL1β and the bacterial membrane component LPS. In vitro HDAC inhibition (HDACi) in colonic epithelial cells generated a strong, NF-κB-dependent enhancement of EcN- and LPS-induced hBD2 expression, but also of the pro-inflammatory cytokine IL8. For IL1β-induced hBD2, the observed augmentation seems to be mediated by additional transducing factors and conditions depending on which HDACs are inhibited. In the case of IL1β, the enhancing effect of HDACi on hBD2 could be evinced in a second colonic epithelial cell line. In an effort to closer mimic the in vivo situation, an ex vivo human colonic biopsy culture has been established with almost identical culture conditions using IBD and healthy control tissue. This was aimed to allow a comparison to the in vitro results, since it is of substantial importance to learn how a more complex, non-tumorous human tissue compound reacts to HDACi. Strikingly, in this context, an opposing impact of HDACi on EcN-stimulated hBD2 expression was observed. Inhibiting HDAC function using pan-HDAC inhibitors hindered hBD2 expression instead of enhancing it, but did not impede IL8 expression. Whether these contrary results could be due to the malignant nature of the in vitro cell lines was investigated using ex vivo treated human colorectal cancer tissue showing the same response as non-cancerous intestinal biopsies. In addition, first insights into the reactivity of a primary, non-transformed gingival epithelial cell line towards HDACi showed a comparable hBD2 response upon IL1β-stimulation as did the cancerous intestinal cell lines. Furthermore, ex vivo fold induction levels of hBD2 in CD patients have been reduced hinting towards a disturbance in hBD2 inducibility in response to EcN. In this study, differential intestinal mRNA expression patterns have been unveiled for class I HDACs. Importantly, a strong regulatory influence of HDACs on the expression of hBD2 could be demonstrated. The simultaneous upregulation of IL8 in epithelial cells and the missing downregulation of the same in biopsy culture under HDACi, advises caution in considering HDACi as therapeutic in IBD. Furthermore, a dependency of the HDACi-induced hBD2 enhancement on NF-κB could be found. Utilizing different culture approaches, the obtained results argue for a cellular context-dependent modulation of the epigenetic regulation of hBD2 expression by HDACs. Overall, this work promotes the understanding of epigenetics as the conjoining integrative mechanism between genome and environment, bridging the way to answering many yet elusive questions in the pathogenesis of IBD