RICERCA ITALIANA     

Programmi di ricerca simili:

• 1 - Basi genetiche e molecolari della patogenicità batterica
• 2 - Interazioni batterio-cellula ospite: analisi genetica e molecolare di meccanismi di virulenza di patogeni enterici di rilevanza clinica con particolare riferimento alla loro capacità di alterare a proprio vantaggio la risposta immune innata dell’ospite.
• 3 - Studio della virulenza di batteri intracellulari: aspetti molecolari ed immunologici.
• 4 - Rapporto ospite parassita nelle infezioni da clamidie e spirochete: immunità naturale e metabolismo lipidico studiati con tecniche convenzionali e con DNA microarray
• 5 - Patogenesi molecolare delle malattie del motoneurone come tool per l’identificazione di nuovi approcci terapeutici biomolecolari e cellulari
• 6 - Analisi delle mappe trascrizionali e delle variazioni di moduli funzionali nel corso del differenziamento mieloide umano normale
• 7 - Legionella pneumophila come patogeno emergente in Sanità Pubblica: nuove prospettive per la valutazione del rischio e strategie innovative per la prevenzione e il controllo della contaminazione ambientale
• 8 - Epifillia come espressione della totipotenza cellulare: studio delle basi molecolari e citofisiologiche della competenza meristematica ed embriogenetica.
• 9 - Dallo studio dell’espressione genica globale allo studio della virulenza di Mycobacterium tuberculosis
• 10 - Meccanismi della citochinesi: identificazione di nuovi geni coinvolti nel processo e nella sua regolazione

Classificazione scientifico-disciplinare

• Area scientifico disciplinare: Scienze biologiche
  • MICROBIOLOGIA GENERALE
• Area scientifico disciplinare: Scienze mediche
  • MICROBIOLOGIA E MICROBIOLOGIA CLINICA

Classificazione brevettuale

• CHEMISTRY; METALLURGY
  • BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
    • MICRO-ORGANISMS OR ENZYMES; COMPOSITIONS THEREOF (biocides, pest repellants or attractants, or plant growth regulators, containing micro-organisms, viruses, microbial fungi, enzymes, fermentates or substances produced by or extracted from micro-organisms or animal material A01N63/00; food compositions A21, A23; medicinal preparations A61K; chemical aspects of, or use of materials for, bandages, dressings, absorbent pads or surgical articles A61L; fertilisers C05); PROPAGATING, PRESERVING OR MAINTAINING MICRO-ORGANISMS (preservation of living parts of humans or animals A01N1/02); MUTATION OR GENETIC ENGINEERING; CULTURE MEDIA (micro-biological testing media C12Q)

Classificazione geografica

• Regione: Campania

Bibliografia

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2) Caugant, D.A., Hoiby, E.A., Magnus, P., Scheel, O., Hoel, T., Bjune, G., Wedege, E., Eng, J., and Froholm, LO. (1994). Asymptomatic carriage of Neisseria meningitidis in a randomly sampled population. J. Clin. Microbiol. 32, 323-330.
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3) Chamaillard M, M Hashimoto, Y Horie, Y Masumoto, S Qiu, L Saab, Y Ogura, A Kawasaki, K Fukase, S Kusumoto, MA Valvano, SJ Foster, TW Mak, G Nunez, N Inohara. 2003. An essential role for NOD1 in host recognition of bacterial peptidoglycan conyaining diaminopimelic acid. Nat Immunol 4: 702-7.
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4) Girardin SE, IG Boneca, J Viala, M Chamaillard, A Labigne, G Thomas, DJ Philpott, PJ Sansonetti. 2003a. Nod2 is a general sensor of peptidoglycan through muramyl dipeptide (MDP) detection. J Biol Chem 278: 8869-72.
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5) Girardin SE, IG Boneca, LAM Carneiro, A Antignac, M Jehanno, J Viala, K Tedin, MK Taha, A Labigne, U Zahringer, AJ Coyle, PS DiStefano, J Bertin, PJ Sansonetti, DJ Philpott. 2003b. Nod1 detects a unique muropeptide from Gram-negative bacterial peptidoglycan. Science 300: 1584-7.
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6) Hauck, C.R., and Meyer, T.F. (2003). 'Small' talk: Opa proteins as mediators of Neisseria-host-cell communication. Curr. Opin. Microbiol. 6, 43-49.
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7) Hoshino K, Takeuchi O, Kawai T, Sanjo H, Ogawa T, Takeda Y, Takeda K, S Akira. 1999. Cutting edge/ Toll-Like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product. J Immunol 162: 3749-52.
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8) Hugot JP, M Chamaillard, H Zouali, S Lesage, JP Cezard, J Belaiche, S Almer, C Tysk, CA O'Morain, M Gassul, V Binder, Y Finkel, A Cortot, R Modigliani, P Laurent-Puig, C Gower-Rousseau, J Macry, JF Colombel, M Sahbatou, G Thomas. 2001. Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease. Nature 411: 599-603.
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9) Inohara N, G Nunez. 2003. NODs: intracellular proteins involved in inflammation and apoptosis. Nat Rev Immunol 3: 371-82.
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10) Inohara N, T Koseki, L Del Peso, Y Hu, C Yee, S Chen, R Carrio, J Merino, D Liu, J Ni. 1999. Nod1, an Apaf-1-like activator of caspase-9 and nuclear factor-kappaB. J Biol Chem 274: 14560-7.
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11) Jedrzejas MJ. 2004. Extracellular virulence factors of Streptococcus pneumoniae. Front Biosci. 9:891-914.
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12) Koedel U, Scheld WM, Pfister HW. 2002. Pathogenesis and pathophysiology of pneumococcal meningitis. The Lancet Infect. Dis. 2: 721-736.
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15) Massari, P., Ram, S., Macleod, H., and Wetzler, L.M. (2003). The role of porins in neisserial pathogenesis and immunity. Trends Microbiol. 11, 87-93.
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16) Medzhitov R. 2001. Toll-like receptors and innate immunity. Nat Rev Immunol 1: 135-45.
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17) Merz, A.J., and So, M. (2000). Interactions of pathogenic neisseriae with epithelial cell membranes. Annu. Rev. Cell. Dev. Biol. 16, 423-457.
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18) Meyer, T.F. (1999). Pathogenic neisseriae: complexity of pathogen-host cell interplay. Clin. Infect. Dis. 28, 433-441.
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19) Mitchell TJ. 2000. Virulence factors and the pathogenesis of disease caused by Streptococcus pneumoniae. Res Microbiol. 151:413-419.
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20) Nassif, X., Bourdoulous, S., Eugene, E., and Couraud, P.O. (2002). How do extracellular pathogens cross the blood-brain barrier? Trends Microbiol. 10, 227-232.
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21) Nassif, X., Pujol, C., Morand, P., and Eugene, E. (1999). Interactions of pathogenic Neisseria with host cells. Is it possible to assemble the puzzle? Mol. Microbiol. 32, 1124-1132.
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22) Ogura Y, DK Bonen, N Inohara, DL Nicolae, FF Chen, R Ramos, H Britton, T Moran, R Karaliuskas, RH Duerr, JP Achkar, SR Brant, TM Bayless, BS Kirschner, SB Hanauer, G Nunez, JH Cho. 2001b. A frameshift mutation in NOD2 associated with the susceptibility to Crohn's disease. Nature 411: 603-6.
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23) Pagliarulo, C., Salvatore, P., De Vitis L.R., Colicchio, R., Monaco, C., Tredici, M., Talà, A., Bardaro, M., Lavitola, A., Bruni, C.B. and Alifano, P. (2004). Regulation and differential expression of gdhA encoding NADP-specific glutamate dehydrogenase in Neisseria meningitidis clinical isolates. Mol. Microbiol. 51, 1757-1772.
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24) Parkhill, .J, Achtman, M., James, K.D., et al. (2000). Complete DNA sequence of a serogroup A strain of Neisseria meningitidis Z2491. Nature 404, 502-506.
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25) Perdomo JJ, P Gounon, PJ Sansonetti. 1994a. Polymorphonuclear leukocyte transmigration promotes invasion of colonic epithelial monolayer by Shigella flexneri. J Clin Invest 93: 633-43.
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26) Philpott DJ, S Yamaoka, A Israel, PJ Sansonetti. 2000. Invasive Shigella flexneri activates NF-kB through an LPS-dependent innate intracellular response and leads to IL-8 expression in epithelial cells. J Immunol 165: 903-14.
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27) Pujol, C., Eugene, E., Morand, P., and Nassif, X. (2000). Do pathogenic neisseriae need several ways to modify the host cell cytoskeleton? Microbes Infect. 2, 821-827.
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28) Speth C, Dierich MP, Gasque P. 2002. Neuroinvasion by pathogens: a key role of the complement system. Mol. Immunol. 38: 669-679.
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29) Sun, Y.H., Bakshi, S., Chalmers, R. and Tang, C.M. (2000) Functional genomics of Neisseria meningitidis pathogenesis. Nat. Med. 6, 1269-1273.
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30) Tattoli I, A Cersini, LAM Carneiro, E Ferraro, G Rossi, MC Martino, ME De Stefano, C Parquet, D Mengin-Lecreulx, DJ Philpott, F Cecconi, AJ Coyle, J Bertin, ML Bernardini. 2004. Nod1, peptidoglycan, and NF-kB govern the balance between survival and apoptosis in infected epithelial cells. Submitted.
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31) Tettelin, H., Saunders, N.J., Heidelberg, J., et al. (2000). Complete genome sequence of Neisseria meningitidis serogroup B strain MC58. Science 287, 1809-1815.
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32) Zychlinsky A, C Fitting, JN Cavaillon, PJ Sansonetti. 1994. Inteleukin 1 is released by macrophages during apoptosis induced by Shigella flexneri. J Clin Invest 94: 1328-34.

Parole Chiave

MICROBIOLOGIA MOLECOLARE; MICROBIOLOGIA CELLULARE; PATOGENESI BATTERICA; ESPRESSIONE GENICA; FATTORI DI VIRULENZA