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Diet as a strategy for type 1 diabetes prevention

Cellular & Molecular Immunology 2018年第1期15卷 1-4页

作者： Flavia Prodam Annalisa Chiocchetti umberto dianzani Department of Health Sciences Universitàdel Piemonte OrientaleNovara28100Italy

The increasing incidence of type 1 diabetes mellitus(T1DM)in children represents one of the major worldwide health concerns.It is widely thought that T1DM is caused by the autoimmune destruction of insulin-producingβcells in the pancreas due to an aberrant T-cell immune response.To date,there are no effective therapeutic strategies to prevent T1DM,as its clinical symptoms become apparent only when mostβcells have already been destroyed.Furthermore,clinical trials for the prevention of T1DM in children at risk have all been unsuccessful to date.Intriguingly,recent studies have implicated alterations in the gut microbial flora(that is,microbiota)as a potential etiological factor for T1DM,raising the possibility that interfering with the microbes populating our body could represent a promising approach to prevent or manage T1DM.New evidence strongly supporting this hypothesis comes from a milestone study by Mariño et al.,1 which shows that a diet capable of modulating the activity of the gut microbiota can indeed inhibit the disease onset in a mouse model of T1DM.Overall,these findings pave the way for the development of food-based dietary approaches for preventing high-risk children from developing T1DM.

关键词： prevention alterations destroyed

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The Yin-Yang of osteopontin in nervous system diseases: damage versus repair

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Neural Regeneration Research 2021年第6期16卷 1131-1137页

作者： Giuseppe Cappellano Domizia Vecchio Luca Magistrelli Nausicaa Clemente Davide Raineri Camilla Barbero Mazzucca Eleonora Virgilio umberto dianzani Annalisa Chiocchetti Cristoforo Comi Department of Health Sciences Interdisciplinary Research Center of Autoimmune Diseases(IRCAD)University of Piemonte OrientaleNovaraItaly Center for Translational Research on Autoimmune and Allergic Disease-CAAD University of Piemonte OrientaleNovaraItaly Department of Translational Medicine Neurology UnitInterdisciplinary Research Center of Autoimmune Diseases(IRCAD)University of Piemonte OrientaleNovaraItaly PhD Program in Clinical and Experimental Medicine and Medical Humanities University of InsubriaVareseItaly

Osteopontin is a broadly expressed pleiotropic protein,and is attracting increased attention because of its role in the pathophysiology of several inflammatory,degenerative,autoimmune,and oncologic diseases.In fact,in the last decade,several studies have shown that osteopontin contributes to tissue damage not only by recruiting harmful inflammatory cells to the site of lesion,but also increasing their survival.The detrimental role of osteopontin has been indeed well documented in the context of different neurological conditions(i.e.,multiple sclerosis,Parkinson’s,and Alzheimer’s diseases).Intriguingly,recent findings show that osteopontin is involved not only in promoting tissue damage(the Yin),but also in repair/regenerative mechanisms(the Yang),mostly triggered by the inflammatory response.These two apparently discordant roles are partly related to the presence of different functional domains in the osteopontin molecule,which are exposed after thrombin or metalloproteases cleavages.Such functional domains may in turn activate intracellular signaling pathways and mediate cell-cell and cell-matrix interactions.This review describes the current knowledge on the Yin and Yang features of osteopontin in nervous system diseases.Understanding the mechanisms behind the Yin/Yang would be relevant to develop highly specific tools targeting this multifunctional protein.

关键词： Alzheimer’s disease cytokine immunity microglia multiple sclerosis neuroinflammation neuroprotection neurotoxicity Parkinson’s disease Spp1 stroke

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Genomic and functional evaluation of TNFSF14 in multiple sclerosis susceptibility

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Journal of Genetics and Genomics 2021年第6期48卷 497-507页

作者： Miriam Zuccala Nadia Barizzone Elena Boggio Luca Gigliotti Melissa Sorosina Chiara Basagni Roberta Bordoni Ferdinando Clarelli Santosh Anand Eleonora Mangano Domizia Vecchio Elena Corsetti Serena Martire Simona Perga Daniela Ferrante Alberto Gajofatto Andrei Ivashynka Claudio Solaro Roberto Cantello Vittorio Martinelli Giancarlo Comi Massimo Filippi Federica Esposito Maurizio Leone Gianluca De Beilis umberto dianzani Filippo Martinelli-Boneschi Sandra D’Alfonso Department of Health Sciences Center on Autoimmune and Allergic Diseases(CAAD)UPOUniversity of Eastern PiedmontA.AvogadroNovara 28100Italy Consorzio Interuniversitario di Biotecnologie(CIB) Trieste 34149Italy Laboratory of Human Genetics of Neurological Disorders Institute of Experimental NeurologyDivision of NeurosciencesIRCCS San Raffaele Scientific InstituteMilan 20132Italy National Research Council of Italy Institute for Biomedical TechnologiesSegrateMilan 20090Italy Department of Genetic Medicine and Development(GEDEV) Faculty of MedicineUniversity of Geneva Medical SchoolGeneva 1211Switzerland Department of Informatics Systems and Communications(DISCo)University of Milano-BicoccaMilan 20126Italy MS Centre SCDU NeurologyAOU Maggiore della CaritàNovara 28100Italy Department of Translational Medicine Interdisciplinary Research Center of Autoimmune Diseases(IRCAD)University of Eastern PiedmontNovaraAvogadro UniversityNovara 28100Italy Neuroscience Institute Cavalieri Ottolenghi OrbassanoTurin 10043Italy Neurobiology Unit Neurology-CReSM(Regional Referring Center of Multiple Sclerosis)AOU San Luigi GonzagaOrbassanoTurin 10043Italy Department of Neuroscience‘Rita Levi Montalcini’ University of TurinTurin 10126Italy Department of Neuroscience Biomedicine and Movement SciencesUniversity of VeronaVerona 37134Italy UO Neurologia Fondazione IRCCS Casa Sollievo della Sofferenza San Giovanni RotondoFoggia 71013Italy Centro Recupero e Rieducazione Funzionale“Mons L Novarese” Moncrivello(VC)13040Italy Department of Neurology IRCCS San Raffaele Scientific InstituteMilan 20132Italy Neuroimaging Research Unit Institute of Experimental NeurologyDivision of NeuroscienceIRCCS San Raffaele Scientific InstituteMilan 20132Italy Vita-Salute San Raffaele University Milan 20138Italy Neurophysiology Unit IRCCS San Raffaele Scientific InstituteMilan 20138Italy Dino Ferrari Centre Neuroscience SectionDepartment of Pathophysiology and Transplantation(DEPT)University of MilanMilan 20122

Among multiple sclerosis(MS)susceptibility genes,the strongest non-human leukocyte antigen(HLA)signal in the Italian population maps to the TNFSF14 gene encoding LIGHT,a glycoprotein involved in dendritic cell(DC)maturation.Through fine-mapping in a large Italian dataset(4,198 patients with MS and3,903 controls),we show that the TNFSF14 intronic SNP rs1077667 is the primarily MS-associated variant in the region.Expression quantitative trait locus(e QTL)analysis indicates that the MS risk allele is significantly associated with reduced TNFSF14 messenger RNA levels in blood cells,which is consistent with the allelic imbalance in RNA-Seq reads(P<0.0001).The MS risk allele is associated with reduced levels of TNFSF14 gene expression(P<0.01)in blood cells from 84 Italian patients with MS and 80 healthy controls(HCs).Interestingly,patients with MS are lower expressors of TNFSF14 compared to HC(P<0.007).Individuals homozygous for the MS risk allele display an increased percentage of LIGHT-positive peripheral blood myeloid DCs(CD11 c+,P=0.035)in 37 HCs,as well as in in vitro monocyte-derived DCs from 22 HCs(P=0.04).Our findings suggest that the intronic variant rs1077667 alters the expression of TNFSF14 in immune cells,which may play a role in MS pathogenesis.

关键词： Multiple sclerosis TNFSF14 LIGHT Fine-mapping analysis SNV

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Albumin nanoformulations as an innovative solution to overcome doxorubicin chemoresistance

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Cancer Drug Resistance 2021年第1期4卷 192-207页

作者： Federica Bessone Chiara dianzani Monica Argenziano Luigi Cangemi Rita Spagnolo Federica Maione Enrico Giraudo Roberta Cavalli Department of Drug Science and Technology University of TurinTurin 10125Italy Laboratory of Tumor microenvironment Candiolo Cancer Institute-FPOIRCCSCandiolo 10060Italy

Aim:Resistance to chemotherapy is a major limiting factor that hamper the effectiveness of anticancer therapies.Doxorubicin is an antineoplastic agent used in the treatment of a wide range of cancers.However,it presents several limitations such as dose-dependent cardiotoxicity,lack of selectivity for tumor cells,and induced cell resistance.Nanotechnology represents a promising strategy to avoid these drawbacks.In this work,new albumin-based nanoparticles were formulated for the intracellular delivery of doxorubicin with the aim to overcome cancer drug resistance.Methods:Glycol chitosan-coated and uncoated albumin nanoparticles were prepared with a tuned coacervation method.The nanoformulations were in vitro characterized evaluating the physicochemical parameters,morphology,and in vitro release kinetics.Biological assays were performed on A2780res and EMT6 cells from human ovarian carcinoma and mouse mammary cell lines resistant for doxorubicin,respectively.Results:Cell viability assays showed that nanoparticles have higher cytotoxicity than the free drug.Moreover,at low concentrations,both doxorubicin-loaded nanoparticles inhibited the cell colony formation in a greater extent than drug solution.In addition,the cell uptake of the different formulations was investigated by confocal microscopy and by the HPLC determination of doxorubicin intracellular accumulation.The nanoparticles were rapidly internalized in greater extent compared to the free drug.Conclusion:Based on these results,doxorubicin-loaded albumin nanoparticles might represent a novel platform to overcome the mechanism of drug resistance in cancer cell lines and improve the drug efficacy.

关键词： Albumin nanoparticles doxorubicin glycol chitosan drug resistance ovarian and breast cancer

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Solid lipid nanoparticles delivering anti-inflammatory drugs to treat inflammatory bowel disease: Effects in an in vivo model

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World Journal of Gastroenterology 2017年第23期23卷 4200-4210页

作者： Chiara dianzani Federica Foglietta Benedetta Ferrara Arianna Carolina Rosa Elisabetta Muntoni Paolo Gasco Carlo Della Pepa Roberto Canaparo Loredana Serpe Department of Drug Science and Technology University of Torino Nanovector s.r.l

AIM To improve anti-inflammatory activity while reducing drug doses, we developed a nanoformulation carrying dexamethasone and butyrate.METHODS Dexamethasone cholesteryl butyrate-solid lipid nanoparticles(Dx Cb-SLN) were obtained with the warm microemulsion method. The anti-inflammatory activity of this novel nanoformulation has been investigated in vitro(cell adhesion to human vascular endothelial cells and pro-inflammatory cytokine release by lipopolysaccharideinduced polymorphonuclear cells) and in vivo(disease activity index and cytokine plasma concentrations in a dextran sulfate sodium-induced mouse colitis) models. Each drug was also administered separately to compare its effects with those induced by their co-administration in SLN at the same concentrations.RESULTS Dx Cb-SLN at the lowest concentration tested(Dx 2.5 nmol/L and Cb 0.1 μmol/L) were able to exert a more than additive effect compared to the sum of the individual effects of each drug, inducing a significant in vitro inhibition of cell adhesion and a significant decrease of pro-inflammatory cytokine(IL-1β and TNF-α) in both in vitro and in vivo models. Notably, only the Dx Cb nanoformulation administration was able to achieve a significant cytokine decrease compared to the cytokine plasma concentration of the untreated mice with dextran sulfate sodium-induced colitis. Specifically, Dx Cb-SLN induced a IL-1β plasma concentration of 61.77% ± 3.19%, whereas Dx or Cb used separately induced a concentration of 90.0% ± 2.8% and 91.40% ± 7.5%, respectively; Dx Cb-SLN induced a TNF-α plasma concentration of 30.8% ± 8.9%, whereas Dx or Cb used separately induced ones of 99.5% ± 4.9% and 71.1% ± 10.9%, respectively.CONCLUSION Our results indicate that the co-administration of dexamethasone and butyrate by nanoparticles may be beneficial for inflammatory bowel disease treatment.

关键词： Nanoparticles Dexamethasone 丁酸盐煽动性的肠疾病药交货系统

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