Sustainable exploitation of paper mill wastes: a resource to re-use in the paper factory

In the papermaking industry, billions of tonnes of paper mill wastes are globally produced as wastes every year. These include cellulosic and inorganic sludges, which are traditionally landfilled, leading to environmental and economic issues. For these reasons, it is urgent to develop new sustainable strategies to exploit these fractions. Up to now, these sludges have been exploited i) for land application (as soil amendment/substrate), ii) for energy recovery and iii) for the production of bio-composites. However, the above possibilities involve the direct use of the bulk wastes, without fractionating/exploiting each feedstock component. In the perspective of the valorisation of the different components, the present investigation has considered different strategies: i) a thermal treatment, ii) an alkaline and iii) a mechanical one, aimed at the fractionation and recovery of the two main components of cellulosic and inorganic sludge, cellulose and calcium carbonate, respectively, that could be advantageously reused within the same papermaking process

Biomass ethanolysis: process optimization and performances of ethyl levulinate as diesel blendstock

Biomass represents a key asset for renewable energy production in the context of the more and more pressing energetic transition. Moreover, at the present, the issue of how to store a convenient amount of energy on board of electric vehicles is still a challenge and electric vehicles perspectives are limited to passenger cars and very small-range trucks, significant amount of time being necessary to define the eventual appropriate electric storage system to be employed in heavy transport, as well in aviation and shipping. In this context alkyl levulinates represent a concrete perspective for partial replacement of fossil fuel with renewable blendstocks. In particular, ethyl levulinate (EL) production by direct acid-catalyzed biomass ethanolysis was studied in order to investigate and optimize this one-step process which involves only renewable starting materials (biomass and bioethanol). In this perspective, the role of the main reaction parameters as the substrate nature and loading, type of the acid catalyst and its concentration, reaction temperature and duration were studied. EL was tested up to high concentrations in a mixture with diesel fuel in a small single-cylinder air-cooled diesel engine, to verify the engine and emission performances of the different blend compositions respect to those ascertained with a conventional diesel fuel

Mapping genetic determinants of host susceptibility to Pseudomonas aeruginosa lung infection in mice.

Background: P. aeruginosa is one of the top three causes of opportunistic human bacterial infections. The remarkable variability in the clinical outcomes of this infection is thought to be associated with genetic predisposition. However, the genes underlying host susceptibility to P. aeruginosa infection are still largely unknown. Results: As a step towards mapping these genes, we applied a genome wide linkage analysis approach to a mouse model. A large F2 intercross population, obtained by mating P. aeruginosa-resistant C3H/HeOuJ, and susceptible A/J mice, was used for quantitative trait locus (QTL) mapping. The F2 progenies were challenged with a P. aeruginosa clinical strain and monitored for the survival time up to 7 days post-infection, as a disease phenotype associated trait. Selected phenotypic extremes of the F2 distribution were genotyped with high-density single nucleotide polymorphic (SNP) markers, and subsequently QTL analysis was performed. A significant locus was mapped on chromosome 6 and was named P. aeruginosa infection resistance locus 1 (Pairl1). The most promising candidate genes, including Dok1, Tacr1, Cd207, Clec4f, Gp9, Gata2, Foxp1, are related to pathogen sensing, neutrophils and macrophages recruitment and inflammatory processes. Conclusions: We propose a set of genes involved in the pathogenesis of P. aeruginosa infection that may be explored to complement human studie

The cystic fibrosis microbiome in an ecological perspective and its impact in antibiotic therapy

The recent focus on the cystic fibrosis (CF) complex microbiome has led to the recognition that the microbes can interact between them and with the host immune system, affecting the disease progression and treatment routes. Although the main focus remains on the interactions between traditional pathogens, growing evidence supports the contribution and the role of emergent species. Understanding the mechanisms and the biological effects involved in polymicrobial interactions may be the key to improve effective therapies and also to define new strategies for disease control. This review focuses on the interactions between microbe-microbe and host-microbe, from an ecological point of view, discussing their impact on CF disease progression. There are increasing indications that these interactions impact the success of antimicrobial therapy. Consequently, a new approach where therapy is personalized to patients by taking into account their individual CF microbiome is suggested.Portuguese Foundation for Science and Technology (FCT), the strategic funding of UID/BIO/04469/2013-CEB and UID/EQU/00511/2013-LEPABE units. This study was also supported by FCT and the European Community fund FEDER, through Program COMPETE, under the scope of the Projects “DNA mimics” PIC/IC/82815/2007, RECI/BBB-EBI/0179/2012 (FCOMP-01-0124-FEDER-027462), “BioHealth—Biotechnology and Bioengineering approaches to improve health quality”, Ref. NORTE-07-0124-FEDER-000027 and NORTE-07-0124-FEDER-000025—RL2_ Environment and Health, co-funded by the Programa Operacional Regional do Norte (ON.2 – O Novo Norte), QREN, FEDER. The authors also acknowledge the grant of Susana P. Lopes (SFRH/BPD/95616/2013) and of the COST-Action TD1004: Theragnostics for imaging and therapy

CXCL10 levels at hospital admission predict COVID-19 outcome- hierarchical assessment of 53 putative inflammatory biomarkers in an observational study

10.1186/s10020-021-00390-4THIS DATASET IS ARCHIVED AT DANS/EASY, BUT NOT ACCESSIBLE HERE. TO VIEW A LIST OF FILES AND ACCESS THE FILES IN THIS DATASET CLICK ON THE DOI-LINK ABOV

The infection by Helicobacter pylori expressing CagA is highly prevalent in women with autoimmune thyroid disorders

H. pylori infection is putatively associated with extra-digestive disorders and may also play a role in the development of autoimmune thyroid diseases (ATD). It was recently found that monoclonal antibodies to an H. pylori strain with cagA-positivity reacted with follicular cells of the thyroid gland, and that an H. pylori organism possessing the cag pathogenicity island carried a gene encoding for an endogenous peroxidase. The aims of this study was (1); To ascertain whether the infection by strains endowed with an increased inflammatory potential (those expressing CagA) could further enhance the risk of developing ATD (2); To verify the possible existence of an immune cross-reactivity between autoantibodies to peroxidase and thyroglobulin and H. pylori antigens (3). To establish whether thyroid colloid antigens could cross-react with an anti-H. pylori serum. The study was partly designed retrospectively. We examined 41 consecutive women with ATD, and, as a control, 33 consecutive age- and socio-economic class-matched women without autoimmune thyroid disorders, living in the same area as patients, occurred at the same institution in the same period (six months). Both patients and controls were examined serologically for H. pylori infection and CagA status by Western blotting. Some serum samples were absorbed with H. pylori to determine whether the antibody levels decreased. Colloid proteins were resolved electrophoretically and matched with a hyperimmune serum raised in rabbits against a CagA-positive H. pylori. Thirty-two patients (78.0%) tested seropositive for H. pylori infection, vs. 16 controls (48.4%) (P = 0.008, OR = 3.78, RR = 1.61). The prevalence of anti-CagA antibodies was 71.8% in infected patients, and 50% in infected controls (P = 0.161, n.s.). The overall prevalence of infection by CagA-positive H. pylori was significantly higher in patients with ATD (23/41, or 56.0%) than that in controls (8/33, or 24.2%) (P = 0.006, OR = 3.99, RR = 2.31). The other tests gave negative or inexplicable results. In conclusion: CagA-positive H. pylori infection increases the risk of ATD development

WS10.5 Pseudomonas aeruginosa adaptation as a potential risk factor to the progression of cystic fibrosis airway disease in mice and humans

Objectives: CF is characterized by loss of pulmonary function and tissue injury. As the disease progresses, P. aeruginosa adapts to the host and dramatically modifies its phenotype; however, it is still unclear if and how bacterial adaptation influences pathogenesis and disease development. Methods: Initially-acquired and CF-adapted P. aeruginosa clonal variants were challenged in C57Bl/6 and CF ko mice after their inclusion in agar beads. Mice were evaluated for bacterial count, lung histopathology, markers of inflammation and tissue damage. Patho-adaptive traits of P. aeruginosa isolated from CF patients airways were correlated with clinical scores. Results: Different to P. aeruginosa initially-acquired strains, CF-adapted variants caused long-term chronic infection in mice by shaping the immune response and activating pathways relevant to tissue damage and remodelling. At an advanced stage of a P. aeruginosa infection, murine airways displayed hallmarks of remodelling and fibrosis, including epithelial hyperplasia and structure degeneration, goblet cell metaplasia, collagen deposition, elastin degradation and several markers of tissue damage. In mice, these pathologic traits are only partially dependent on the CFTR genetic background. In CF patients, we observed correlation between P. aeruginosa patho-adaptive traits and inflammation, remodelling processes and lung functions suggesting exploitable disease markers. Conclusion: We conclude that bacterial adaptation may be a potential risk factor in the progression of airway disease and a critical success determinant for reproducing the human disease in mice. Supported by Italian CF Research Foundation

Pseudomonas aeruginosa exploits lipid A and muropeptides modification as a strategy to lower innate immunity during chronic lung infection in cystic fibrosis

Pseudomonas aeruginosa can establish life-long airways chronic infection in patients with cystic fibrosis (CF) with pathogenic variants distinguished from initially acquired strain. Here, we analysed chemical and biological activity of P. aeruginosa Pathogen-Associated Molecular Patterns (PAMPs) in clonal strains, including mucoid and non-mucoid phenotypes, isolated during a period of up to 7.5 years from a CF patient. Chemical structure by MS spectrometry defined lipopolysaccharide (LPS) lipid A and peptidoglycan (PGN) muropeptides with specific structural modifications temporally associated with CF lung infection. Gene sequence analysis revealed novel mutation in pagL, which supported lipid A changes. Both LPS and PGN had different potencies when activating host innate immunity via binding TLR4 and Nod1. Significantly higher NF-kB activation, IL-8 expression and production were detected in HEK293hTLR4/MD2-CD14 and HEK293hNod1 after stimulation with LPS and PGN respectively, purified from early P. aeruginosa strain as compared to late strains. Similar results were obtained in macrophages-like cells THP-1, epithelial cells of CF origin IB3-1 and their isogenic cells C38, corrected by insertion of cystic fibrosis transmembrane conductance regulator (CFTR). In murine model, altered LPS structure of P. aeruginosa late strains induces lower leukocyte recruitment in bronchoalveolar lavage and MIP-2, KC and IL-1beta cytokine levels in lung homogenates when compared with early strain. Histopathological analysis of lung tissue sections confirmed differences between LPS from early and late P. aeruginosa. Finally, in this study for the first time we unveil how P. aeruginosa has evolved the capacity to evade immune system detection, thus promoting survival and establishing favourable conditions for chronic persistence. Our findings provide relevant information with respect to chronic infections in CF

Host genetic background influences the response to the opportunistic Pseudomonas aeruginosa infection altering cell-mediated immunity and bacterial replication

Pseudomonas aeruginosa is a common cause of healthcare-associated infections including pneumonia, bloodstream, urinary tract, and surgical site infections. The clinical outcome of P. aeruginosa infections may be extremely variable among individuals at risk and patients affected by cystic fibrosis. However, risk factors for P. aeruginosa infection remain largely unknown. To identify and track the host factors influencing P. aeruginosa lung infections, inbred immunocompetent mouse strains were screened in a pneumonia model system. A/J, BALB/cJ, BALB/cAnNCrl, BALB/cByJ, C3H/HeOuJ, C57BL/6J, C57BL/6NCrl, DBA/2J, and 129S2/SvPasCRL mice were infected with P. aeruginosa clinical strain and monitored for body weight and mortality up to seven days. The most deviant survival phenotypes were observed for A/J, 129S2/SvPasCRL and DBA/2J showing high susceptibility while BALB/cAnNCrl and C3H/HeOuJ showing more resistance to P. aeruginosa infection. Next, one of the most susceptible and resistant mouse strains were characterized for their deviant clinical and immunological phenotype by scoring bacterial count, cell-mediated immunity, cytokines and chemokines profile and lung pathology in an early time course. Susceptible A/J mice showed significantly higher bacterial burden, higher cytokines and chemokines levels but lower leukocyte recruitment, particularly neutrophils, when compared to C3H/HeOuJ resistant mice. Pathologic scores showed lower inflammatory severity, reduced intraluminal and interstitial inflammation extent, bronchial and parenchymal involvement and diminished alveolar damage in the lungs of A/J when compared to C3H/HeOuJ. Our findings indicate that during an early phase of infection a prompt inflammatory response in the airways set the conditions for a non-permissive environment to P. aeruginosa replication and lock the spread to other organs. Host gene(s) may have a role in the reduction of cell-mediated immunity playing a critical role in the control of P. aeruginosa infection. These results now provide a basis for mapping genomic regions underlying host susceptibility to P. aeruginosa infection