Developed skills and lines of research
Maria Cristina Dechecchi graduated in Biological Sciences at the University of Bari and later specialized in Biochemistry and Clinical Chemistry at the University of Brescia. In 2006 she became senior biologist at the Verona University Hospital. She has extensive experience in the molecular diagnosis of cystic fibrosis and has been conducting research on pulmonary inflammation in CF for many years. Her work has focused on certain anti-inflammatory molecules from the iminosugar family, which she has recently optimized for therapeutic applications in CF-related inflammation.
Projects funded by FFC Ricerca as Principal Investigator or as Research Manager
FFC#20/2019
Evaluation of anti-inflammatory treatments for CF lung disease in murine models of lung infection in vivo: insights on the anti-inflammatory effect of β-sitosterol and anti-inflammatory/anti-infective activity of L-miglustat
FFC#23/2018
Evaluation of anti-inflammatory treatments for CF lung disease in murine models of lung infection in vivo
FFC#22/2015
A systematic investigation of miglustat-derivative iminosugar clusters as possible anti-inflammatory agents for Cystic Fibrosis lung disease
FFC#14/2012
Structure-activity relationships (SAR) of neoglycoconjugates derived from deoxynojirimycin as possible therapeutic agents for Cystic Fibrosis lung disease, by modulating the metabolism of sphingolipids
FFC#16/2010
Modulation of sphingolipid metabolism as a strategy for the treatment of CF lung inflammation
FFC#12/2008
Anti-inflammatory effect of miglustat: sphingolipid ceramide metabolism as a therapeutic target for CF lung disease
FFC#16/2006
Effect of correctors of defective CFTR on the Pseudomonas aeruginosa-dependent inflammatory response in respiratory epithelial cells
FFC#14/2004
Interaction in vitro between cystic fibrosis pathogens and epithelial cells expressing the cystic fibrosis transmembrane conductance regulator (CFTR)
Projects financed by FFC Ricerca as a partner
FFC#19/2009
Role of CFTR-Connexin interaction on PGE2 signaling and inflammation: implication for cystic fibrosis
Publications from FFC Research projects
Dechecchi MC, Nicolis E, Bezzerri V, et al. MPB-07 reduces the inflammatory response to Pseudomonas aeruginosa in cystic fibrosisbronchial cells. Am J Respir Cell Mol Biol, 2007 May, 36(5):615-24.
Dechecchi MC, Nicolis E, Norez C, et al. Anti-inflammatory effect of miglustat in bronchial epithelial cells. J Cyst Fibros, 2008 Nov, 7(6):555-65. doi: 10.1016/j.jcf.2008.06.002.
Dechecchi MC, Nicolis E, Mazzi P, et al. Modulators of sphingolipid metabolism reduce lung inflammation. Am J Respir Cell Mol Biol, 2011 Oct, 45(4):825-33. doi: 10.1165/rcmb.2010-0457OC.
Dechecchi MC et al. Pharmacological modulators of sphingolipid metabolism for the treatment of cystic fibrosis lung inflammation. Cystic Fibrosis INBS Book, 2011.
Galli F, Battistoni A, Gambari R, et al., Oxidative stress and antioxidant therapy in cystic fibrosis. Biochim Biophys Acta. 2012 May;1822(5):690-713. doi: 10.1016/j.bbadis.2011.12.012.
Bezzerri V, Avitabile C, Dechecchi MC, et al. Antibacterial and anti-inflammatory activity of a temporin B peptide analogue on an in vitro model of cystic fibrosis. J Pept Sci, 2014 Oct; 20(10):822-30. doi: 10.1002/psc.2674.
Loberto N, Tebon M, Lampronti I, et al., GBA2-encoded β-glucosidase activity is involved in the inflammatory response to Pseudomonas aeruginosa. PLoS One. 2014 Aug 20;9(8):e104763. doi: 10.1371/journal.pone.0104763. eCollection 2014.
Silvia Munari, Nicoletta Loberto, Massimo Aureli, et al., Neoglycoconjugates Derived from Deoxynojirimycin as Possible Therapeutic Agents for Cystic Fibrosis Lung Disease, by Modulation of the Sphingolipid Metabolism. JSM Genetics and Genomics, short communication, 2016.
Chiricozzi E, Loberto N, Schiumarini D et al. Sphingolipids role in the regulation of inflammatory response: from leukocyte biology to bacterial infection. J Leukoc Biol. 2018 Jan 9. doi: 10.1002/JLB.3MR0717-269R. [Epub ahead of print].
Lampronti I, Dechecchi MC, Rimessi A et al. β-Sitosterol Reduces the Expression of Chemotactic Cytokine Genes in Cystic Fibrosis Bronchial Epithelial Cells. Front Pharmacol. 2017 May 12;8:236. doi: 10.3389/fphar.2017.00236. eCollection 2017.
Purzner T, Purzner J, Buckstaff T, et al. Developmental phosphoproteomics identifies the kinase CK2 as a driver of Hedgehog signaling and a therapeutic target in medulloblastoma. Sci Signal. 2018 Sep 11;11(547). pii: eaau5147. doi: 10.1126/scisignal.aau5147.
Lampronti I, Dechecchi MC, Rimessi A, Bezzerri V, Nicolis E, Guerrini A, Tacchini M, Tamanini A, Munari S, D’Aversa E, Santangelo A, Lippi G, Sacchetti G, Pinton P, Gambari R, Agostini M, Cabrini G. β-Sitosterol Reduces the Expression of Chemotactic Cytokine Genes in Cystic Fibrosis Bronchial Epithelial Cells. Front Pharmacol. 2017 May 12;8:236. doi: 10.3389/fphar.2017.00236. eCollection 2017.
Maria De Fenza, Daniele D’Alonzo, Anna Esposito, et al. Exploring the Effect of Chirality on the Therapeutic Potential of N-alkyl-deoxyiminosugars: Anti-Inflammatory Response to Pseudomonas Aeruginosa Infections for Application in CF Lung Disease. Eur J Med Chem, 175, 63-71 2019 Aug 1