Reduced contamination and infection via inhibition of adhesion of foodborne bacteria to abiotic polystyrene and biotic amoeba surfaces

Adhesion of foodborne pathogens to materials of industrial surfaces is an important step in their transmission through the food chain. Adhesion is also a prerequisite for bacterial colonisation within a host, to enable intracellular invasion. We define a strategy to reduce contamination and infection by Listeria monocytogenes, Campylobacter jejuni and Escherichia coli using an ethanol extract of Alpinia katsumadai seeds (AlpE) and epigallocatechin gallate (EGCG) as anti‐adhesive agents. We show for the first time that AlpE and EGCG reduce adhesion of individual cultures to polystyrene (AlpE, up to 10.6%; EGCG, up to 39.7%) and to the amoeba Acanthamoeba castellanii (AlpE, up to 52.6%; EGCG, up to 53.4%). The combination of AlpE/EGCG significantly reduced C. jejuni adherence to the abiotic (45.5%) and biotic (52.2%) surfaces. Thus, using natural agents from plants at low doses, we can potentially reduce the primary source of food contamination and a frequent source of infections.     

Phosphate recovery from wastewater using engineered superparamagnetic particles modified with layered double hydroxide ion exchangers

An innovative nanocomposite material is proposed for phosphate recovery from wastewater using magnetic assistance. Superparamagnetic microparticles modified with layered double hydroxide (LDH) ion exchangers of various compositions act as phosphate adsorbers. Magnetic separation and chemical regeneration of the particles allows their reuse, leading to the successful recovery of phosphate.     

Characterization of plant food allergens: An overview on physicochemical and immunological techniques

Allergy to plant‐derived foods is a highly complex disorder with clinical manifestations ranging from mild oral, gastrointestinal, and cutaneous symptoms to life‐threatening systemic conditions. This heterogeneity in clinical manifestations has been attributed to different properties of allergenic molecules. Based on this fact, symptom elicitors were grouped into class I and pollinosis‐associated class II food allergens, but clear distinction is rather ambiguous. Moreover, mechanisms underlying food sensitization are not fully understood yet, and food allergy management most often relies on patient's compliance to avoid suspected foods. Therefore, recent efforts aim at the investigation of plant food allergies at the molecular level. This review provides an overview on currently available techniques for allergen characterization and discusses their application for investigation of plant food allergens. Data obtained by an array of physicochemical analyses, such as allergen structure, integrity, aggregation, and stability, need to be linked to results from immunological methods at the level of IgE and T‐cell reactivity. Such knowledge allows the development of computational algorithms to predict allergenicity of novel foods being introduced by biotechnological industry. Furthermore, molecular characterization is an indispensable tool for molecule‐based diagnosis and future development of safer patient‐tailored specific immunotherapy in plant food allergy.     

Cultivation and Hydrothermal Gasification of Microalgae Scenedesmus Obliquus – First Experimental Results

Microalgae (Scenedesmus obliquus) produced in flat panel photobioreactors were converted via supercritical water gasification. The long term aim is to gain higher process efficiency through recycling of byproducts of supercritical water gasification and waste water during the cultivation of microalgae. The first step of the project, the general feasibility of conversion of microalgae Scenedesmus obliquus via supercritical water gasification to a hydrogen‐rich combustible gas is presented. The product gas had a higher heating value and consisted of hydrogen, methane, carbon dioxide, and ethane.     

Immunotherapy in Advanced Prostate Cancer—Light at the End of the Tunnel?

Immunotherapeutic treatment approaches are now an integral part of the treatment of many solid tumors. However, attempts to integrate immunotherapy into the treatment of prostate cancer have been disappointing so far. This is due to a highly immunosuppressive, “cold” tumor microenvironment, which is characterized, for example, by the absence of cytotoxic T cells, an increased number of myeloid-derived suppressor cells or regulatory T cells, a decreased number of tumor antigens, or a defect in antigen presentation. The consequence is a reduced efficacy of many established immunotherapeutic treatments such as checkpoint inhibitors. However, a growing understanding of the underlying mechanisms of tumor–immune system interactions raises hopes that immunotherapeutic strategies can be optimized in the future. The aim of this review is to provide an overview of the current status and future directions of immunotherapy development in prostate cancer. Background information on immune response and tumor microenvironment will help to better understand current therapeutic strategies under preclinical and clinical development.     

Cathepsin X Activity Does Not Affect NK-Target Cell Synapse but Is Rather Distributed to Cytotoxic Granules

Cathepsin X is a lysosomal peptidase that is involved in tumour progression and represents a potential target for therapeutic interventions. In addition, it regulates important functions of immune cells and is implicated in the modulation of tumour cell–immune cell crosstalk. Selective cathepsin X inhibitors have been proposed as prospective antitumour agents to prevent cancer progression; however, their impact on the antitumour immune response has been overlooked. Previous studies indicate that the migration and adhesion of T cells and dendritic cells are affected by diminished cathepsin X activity. Meanwhile, the influence of cathepsin X inhibition on natural killer (NK) cell function has not yet been explored. Here, we examined the localization patterns of cathepsin X and the role of its inhibitors on the cytotoxicity of cell line NK-92, which is used for adoptive cellular immunotherapy in cancer patients. NK-92 cells depend on lymphocyte function-associated antigen 1 (LFA-1) to form stable immunoconjugates with target cells, providing, in this way, optimal cytotoxicity. Since LFA-1 is a substrate for cathepsin X activity in other types of cells, we hypothesized that cathepsin X could disturb the formation of NK-92 immunoconjugates. Thus, we employed cathepsin X reversible and irreversible inhibitors and evaluated their effects on the NK-92 cell interactions with target cells and on the NK-92 cell cytotoxicity. We show that cathepsin X inhibition does not impair stable conjugate formation or the lytic activity of NK-92 cells. Similarly, the conjugate formation between Jurkat T cells and target cells was not affected by cathepsin X activity. Unlike in previous migration and adhesion studies on T cells, in NK-92 cells cathepsin X was not co-localized with LFA-1 at the plasma membrane but was, rather, redistributed to the cytotoxic granules and secreted during degranulation.     

Production of specific structured lipids by enzymatic interesterification: optimization of the reaction by response surface design

Rapeseed oil and capric acid were interesterified in solvent-free media catalyzed by Lipozyme IM from Rhizomucor miehei to produce specific-structured lipids (SSLs). The process was optimized by response surface design concerning the effects of acyl migration and the byproducts of diacylglycerols (DAGs). A five-factor response surface design was used to evaluate the influences of five major factors and their relationships. The five factors were water content (W_c, wt-% based on enzyme used), reaction temperature (T_e, °C), enzyme load (E_l, wt-% based on substrates), reaction time (T_r, h) and substrate ratio (S_r, rapeseed oil/capric acid, mol/mol), varied at three levels together with two star point levels. The net incorporation [Δ(I_f–M_f), in which I_f represents incorporation (1,3-positions) and M_f acyl migration (2-position), and the contents of DAGs were analyzed and calculated. All parameters had strong influence on the net incorporation, and the experimental and predicted values were close. The best fitting quadratic model was determined by regression and backward elimination. The coefficients of determination (R²) of the models were 0.971 for net incorporation and 0.938 for DAG content. Thus, we conclude that the quadratic response models adequately expressed the reaction. Based on the models, the reaction was optimized for the maximum net incorporation and minimum DAG content. The reaction and the control of water content or water activity (Aw) was also discussed.     

pH-Sensing G Protein-Coupled Receptor OGR1 (GPR68) Expression and Activation Increases in Intestinal Inflammation and Fibrosis

Local extracellular acidification occurs at sites of inflammation. Proton-sensing ovarian cancer G-protein-coupled receptor 1 (OGR1, also known as GPR68) responds to decreases in extracellular pH. Our previous studies show a role for OGR1 in the pathogenesis of mucosal inflammation, suggesting a link between tissue pH and immune responses. Additionally, pH-dependent signalling is associated with the progression of intestinal fibrosis. In this study, we aimed to investigate OGR1 expression and OGR1-mediated signalling in patients with inflammatory bowel disease (IBD). Our results show that OGR1 expression significantly increased in patients with IBD compared to non-IBD patients, as demonstrated by qPCR and immunohistochemistry (IHC). Paired samples from non-inflamed and inflamed intestinal areas of IBD patients showed stronger OGR1 IHC staining in inflamed mucosal segments compared to non-inflamed mucosa. IHC of human surgical samples revealed OGR1 expression in macrophages, granulocytes, endothelial cells, and fibroblasts. OGR1-dependent inositol phosphate (IP) production was significantly increased in CD14+ monocytes from IBD patients compared to healthy subjects. Primary human and murine fibroblasts exhibited OGR1-dependent IP formation, RhoA activation, F-actin, and stress fibre formation upon an acidic pH shift. OGR1 expression and signalling increases with IBD disease activity, suggesting an active role of OGR1 in the pathogenesis of IBD.