Elimination de la matière organique biodégradable par ultrafiltration

Les installations de production de la Compagnie des Eaux de banlieue (CEB) au Mont Valérien traitent l'eau de Seine en aval de Paris sur 2 filières de potabilisation comprenant pour la première (50 000 m3/J) une préozonation, une coagulation au sels d'Aluminium (Aqualenc), une décantation (super pulsator Degrémont), une filtration sur sable, une ozonation, une filtration sur charbon actif en grains (CAG) et une désinfection finale au bioxyde de chlore, et pour la deuxième, une filtration lente sur sable (80 000 m3/j) dite filtration "Chabale".Dans le cadre du remplacement de la filière "Chabale", une unité de démonstration (8 m3/h) eomprenaut une addition de charbon actif en poudre (CAP) avant ultrafiltration sur membrane a été mise en route.Dans cette étude, une comparaison du traitement conventionnel physico-chimique de l'usine et du nouveau procédé d'ultrafiltration a été effectuée. Pour cela, un suivi du carbone organique total et une évaluation du potentiel de reviviscence ont été réalisés en différents points des chaînes de traitement. La matière organique biodégradable (MOB) a été mesurée par la méthode Werner (1980).Les premiers résultats montrent :- l'élimination des MOB est comparable pour les différents procédés;- toutefois, la nature des MOB est sensiblement affectée à chaque type de traitement (ozonation, addition de CAP, filtration sur sable ou sur CAG)."Compagnie des Eaux de Banlieue" water facilities located at the Mont-Valérien treat the Seine river water downstream Paris. A first facility (5000 m3/day) includes the following processes : preozonation, coagulation, settling, sand filtration, postozonalion, GAC filtration and a final desinfection (CIO2). A second one consists in a biological sand filtration (80000 m3/day). An ultrafiltration demonstration plant including a CAP addition into the recirculation loop is currently tested on a small scale (8 m3/h) to compare the conventional treatments with new ultrafiltration process.In this study, the TOC removal as well as the biodegradable organic matter (BOM) removal are evaluated on the different processes. The BOM has been assessed by the Werner methodology (1980).During the cool season (october-january) all the biodegradable organic matter were removed by the clarification process (preozonation + coagulation decantation + sand filtration). More than 90 % of the BOM were also removed by the ultrafiltration demonstration plant (including granular activated carbon) although the addition of preozonation slightly increases the effluent BOM concentrations and modifies its composition. 80 % of the dissolved organic compounds were removed by the preozonation + ultrafiltration + powder treatment line. This performance should be compared with the 70 % removal obtained with conventional treatments.This study demonstrate that the combination 03 + UF + CAP can advantageously replace traditional treatment such as preozonation + coagulation clarification + ozonation + granular activated carbon + desinfection

Recombinant Interleukin-24 Lacks Apoptosis-Inducing Properties in Melanoma Cells

IL-24, also known as melanoma differentiation antigen 7 (mda-7), is a member of the IL-10 family of cytokines and is mainly produced by Th2 cells as well as by activated monocytes. Binding of IL-24 to either of its two possible heterodimeric receptors IL-20R1/IL-20R2 and IL-22R/IL-20R2 activates STAT3 and/or STAT1 in target tissues such as lung, testis, ovary, keratinocytes and skin. To date, the physiological properties of IL-24 are still not well understood but available data suggest that IL-24 affects epidermal functions by increasing proliferation of dermal cells. In stark contrast to its “normal” and physiological behaviour, IL-24 has been reported to selectively and efficiently kill a vast variety of cancer cells, especially melanoma cells, independent of receptor expression and Jak-STAT signalling. These intriguing properties have led to the development of adenovirally-expressed IL-24, which is currently being evaluated in clinical trials. Using three different methods, we have analysed a large panel of melanoma cell lines with respect to IL-24 and IL-24 receptor expression and found that none of the investigated cell lines expressed sufficient amounts of functional receptor pairs and therefore did not react to IL-24 stimulation with Jak/STAT activation. Results for three cell lines contrasted with previous studies, which reported presence of IL-24 receptors and activation of STAT3 following IL-24 stimulation. Furthermore, evaluating four different sources and modes of IL-24 administration (commercial recombinant IL-24, bacterially expressed GST-IL-24 fusion protein, IL-24 produced from transfected Hek cells, transiently over-expressed IL-24) no induction or increase in cell death was detected when compared to appropriate control treatments. Thus, we conclude that the cytokine IL-24 itself has no cancer-specific apoptosis-inducing properties in melanoma cells

The role of IL-22 in viral infections: paradigms and paradoxes

Interleukin-22 (IL-22) is a member of the IL-10 family of cytokines. Hematopoietic cells express IL-22, and this cytokine signals through the heterodimeric IL-22 receptor expressed by non-hematopoietic cells. A growing body of evidence points toward a role for IL-22 in a diverse array of biological functions ranging from cellular proliferation, tissue protection and regeneration, and inflammation. In recent years, the role that IL-22 plays in antiviral immune responses has been examined in a number of infection models. Herein, we assess our current understanding of how IL-22 determines the outcome of viral infections and define common mechanisms that are evident from, sometimes paradoxical, findings derived from these studies. Finally, we discuss the potential therapeutic utility of IL-22 manipulation in the treatment and prevention of viral infections and associated pathologies

Crystallization and synchrotron X-ray diffraction studies of human interleukin-22

Human interleukin-22, a novel member of the cytokine family, has been crystallized in hanging drops using the vapour-diffusion technique. Preliminary X-ray diffraction experiments using synchrotron radiation reveal that the protein crystallizes in space group P2(1)2(1)2(1), with unit-cell parameters a = 55.44, b = 61.62, c = 73.43 Angstrom, and diffracts beyond 2.00 Angstrom resolution.58352953

IL-22 mediates goblet cell hyperplasia and worm expulsion in intestinal helminth infection.

Type 2 immune responses are essential in protection against intestinal helminth infections. In this study we show that IL-22, a cytokine important in defence against bacterial infections in the intestinal tract, is also a critical mediator of anti-helminth immunity. After infection with Nippostrongylus brasiliensis, a rodent hookworm, IL-22-deficient mice showed impaired worm expulsion despite normal levels of type 2 cytokine production. The impaired worm expulsion correlated with reduced goblet cell hyperplasia and reduced expression of goblet cell markers. We further confirmed our findings in a second nematode model, the murine whipworm Trichuris muris. T.muris infected IL-22-deficient mice had a similar phenotype to that seen in N.brasiliensis infection, with impaired worm expulsion and reduced goblet cell hyperplasia. Ex vivo and in vitro analysis demonstrated that IL-22 is able to directly induce the expression of several goblet cell markers, including mucins. Taken together, our findings reveal that IL-22 plays an important role in goblet cell activation, and thus, a key role in anti-helminth immunity

Alpha and lambda interferon together mediate suppression of CD4 T cells induced by respiratory syncytial virus

The mechanism by which respiratory syncytial virus (RSV) suppresses T-cell proliferation to itself and other antigens is poorly understood. We used monocyte-derived dendritic cells (MDDC) and CD4 T cells and measured [(3)H]thymidine incorporation to determine the factors responsible for RSV-induced T-cell suppression. These two cell types were sufficient for RSV-induced suppression of T-cell proliferation in response to cytomegalovirus or Staphylococcus enterotoxin B. Suppressive activity was transferable with supernatants from RSV-infected MDDC and was not due to transfer of live virus or RSV F (fusion) protein. Supernatants from RSV-infected MDDC, but not MDDC exposed to UV-killed RSV or mock conditions, contained alpha interferon (IFN-alpha; median, 43 pg/ml) and IFN-lambda (approximately 1 to 20 ng/ml). Neutralization of IFN-alpha with monoclonal antibody (MAb) against one of its receptor chains, IFNAR2, or of IFN-lambda with MAb against either of its receptor chains, IFN-lambdaR1 (interleukin 28R [IL-28R]) or IL-10R2, had a modest effect. In contrast, blocking the two receptors together markedly reduced or completely blocked the RSV-induced suppression of CD4 T-cell proliferation. Defining the mechanism of RSV-induced suppression may guide vaccine design and provide insight into previously uncharacterized human T-cell responses and activities of interferons

IL-22 Is Produced by Innate Lymphoid Cells and Limits Inflammation in Allergic Airway Disease

Interleukin (IL)-22 is an effector cytokine, which acts primarily on epithelial cells in the skin, gut, liver and lung. Both pro- and anti-inflammatory properties have been reported for IL-22 depending on the tissue and disease model. In a murine model of allergic airway inflammation, we found that IL-22 is predominantly produced by innate lymphoid cells in the inflamed lungs, rather than TH cells. To determine the impact of IL-22 on airway inflammation, we used allergen-sensitized IL-22-deficient mice and found that they suffer from significantly higher airway hyperreactivity upon airway challenge. IL-22-deficiency led to increased eosinophil infiltration lymphocyte invasion and production of CCL17 (TARC), IL-5 and IL-13 in the lung. Mice treated with IL-22 before antigen challenge displayed reduced expression of CCL17 and IL-13 and significant amelioration of airway constriction and inflammation. We conclude that innate IL-22 limits airway inflammation, tissue damage and clinical decline in allergic lung disease

IL-22-expressing murine lymphocytes display plasticity and pathogenicity in reporter mice

IL-22 has multiple activities ranging from tissue repair to inflammation. To characterize the pathogenicity and plasticity of cells that produce IL-22 a novel reporter mouse strain was generated. Homeostatic IL-22 reporter expression was observed in intestinal lymphoid cells identified as CD4 T cells and ILC3 cells. In a model of inflammatory bowel disease (IBD), CD4 T cells strongly expressed the IL-22 reporter in mesenteric lymph node. To examine plasticity of IL-22+ T cells, they were purified after generation in vitro or in vivo from inflamed colon, then cultured under Th1, Th2 or Th17 conditions. In vitro-generated IL-22+ CD4 T cells showed relatively durable IL-22 expression under Th1 or Th2 conditions, whereas in vivo generated cells rapidly lost IL-22 expression under these conditions. In vitro-generated cells could not be diverted to express Th1 or Th2 cytokines despite the expression of master regulators. In vivo generated cells could be diverted, at very low frequency, to express Th1 or Th2 cytokines. Both in vitro- and in vivo-generated cells could be induced in vitro to express high levels of IL-17A and IL-17F, assigning them to a Th17 biased class. IL-27 potently downregulated IL-22 expression. To examine IL-22+ T cell pathogenicity, in vitro generated cells were transferred into Rag1-/- mice, retaining modest reporter expression and inducing moderate colitis. In contrast, IL-22 expressers from colitic mice, transferred into secondary hosts, lost reporter expression, acquired high Tbet and modest IFN and IL-17 expression and induced severe colitis. These findings are consistent with a model of strong polarization under optimal in vitro conditions, but a plastic state of T cells in vivo