The most common method to deal with the huge production of municipal wastes is still the disposal in landfills which, however, generates a leachate with high contents of organic and nitrogen pollutants. Requirements must be fixed by law to control leachate release from such landfills, and effective treatment processes and technologies must be applied to reduce its impact on the environment. Biological processes for leachate treatment are discussed in this review, in the former part of which attention is paid to leachate formation and its qualitative and quantitative features, while the latter deals with the state‐of‐the‐art of the most effective biotechnological treatments presently employed. Processes, alternative methods, and technological improvements are compared, with special focus on novel technologies to remove nitrogen pollutants from leachate, highlighting advantages and drawbacks of each treatment.

Stem cell therapies achieved thus this far the most promising results, while immune ablation and standard immunosuppressants did not maintain the premises of preclinical results. The next step will be to generate a feasible and safe clinical approach in order to cure the thousands of patients affected by T1D.

Background: Experimental autoimmune encephalomyelitis (EAE) is the most common animal model of multiple sclerosis (MS), a neuroinflammatory and demyelinating disease characterized by multifocal perivascular infiltrates of immune cells. Although EAE is predominantly considered a T helper 1-driven autoimmune disease, mounting evidence suggests that activated dendritic cells (DC), which are the bridge between innate and adaptive immunity, also contribute to its pathogenesis. Sirtuin 6 (SIRT6), a NAD +-dependent deacetylase involved in genome maintenance and in metabolic homeostasis, regulates DC activation, and its pharmacological inhibition could, therefore, play a role in EAE development. Methods: EAE was induced in female C57bl/6 mice by MOG35-55 injection. The effect of treatment with a small compound SIRT6 inhibitor, administered according to therapeutic and preventive protocols, was assessed by evaluating the clinical EAE score. SIRT6 inhibition was confirmed by Western blot analysis by assessing the acetylation of histone 3 lysine 9, a known SIRT6 substrate. The expression of DC activation and migration markers was evaluated by FACS in mouse lymph nodes. In addition, the expression of inflammatory and anti-inflammatory cytokines in the spinal cord were assessed by qPCR. T cell infiltration in spinal cords was evaluated by immunofluorescence imaging. The effect of Sirt6 inhibition on the migration of resting and activated bone marrow-derived dendritic cells was investigated in in vitro chemotaxis assays. Results: Preventive pharmacological Sirt6 inhibition effectively delayed EAE disease onset through a novel regulatory mechanism, i.e., by reducing the representation of CXCR4-positive and of CXCR4/CCR7-double-positive DC in lymph nodes. The delay in EAE onset correlated with the early downregulation in the expression of CD40 on activated lymph node DC, with increased level of the anti-inflammatory cytokine IL-10, and with a reduced encephalitogenic T cell infiltration in the central nervous system. Consistent with the in vivo data, in vitro pharmacological Sirt6 inhibition in LPS-stimulated, bone marrow-derived DC reduced CCL19/CCL21-and SDF-1-induced DC migration.

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