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Andrea Puhar


Ph.D., Programme “Molecular and Cellular Biology and Pathology”, University of Padua, Italy

Current position

Group Leader, The Laboratory for Molecular Infection Medicine Sweden (MIMS)-The Nordic EMBL Partnership for Molecular Medicine and Department of Molecular Biology, Umeå University, Sweden


Peer-reviewed publications

  1. Boal, F., Puhar, A., Xuereb, J. M., Kunduzova, O., Sansonetti, P. J., Payrastre, B. and Tronchere, H. (2016). PI5P triggers ICAM-1 degradation in shigella infected cells, thus dampening immune cell recruitment. Cell Rep 14(4): 750-759.
    This study shows in vitro and in vivo that the rare phosphoinositide PtdIns5P, which is produced by a bacterial enzyme that is injected into mammalian cells, triggers the internalisation and lysosomal degradation of the cell surface receptor ICAM-1, which dampens immune cell recruitment to sites of infection. This highlights the importance of PtdIns5P in endosomal trafficking.  
  2. Bravo, V., Puhar, A., Sansonetti, P., Parsot, C. and Toro, C. S. (2015). Distinct mutations led to inactivation of type 1 fimbriae expression in Shigella spp. PLoS One 10(3): e0121785.
  3. Puhar, A. and Sansonetti, P. J. (2014). Type III secretion system. Curr Biol 24(17): R784-791. (Corresponding author)
  4. Puhar, A. and Sansonetti, P. J. (2014). Induction of connexin-hemichannel opening. Bio-protocol 4(17): e1220. (Corresponding author) Featured protocol
  5. Puhar, A. and Sansonetti, P. J. (2014). Dye-uptake experiment through connexin hemichannels. Bio-protocol 4(17): e1221. (Corresponding author) Featured protocol
  6. Puhar, A., Tronchere, H., Payrastre, B., Nhieu, G. T. and Sansonetti, P. J. (2013). A Shigella effector dampens inflammation by regulating epithelial release of danger signal ATP through production of the lipid mediator PtdIns5P. Immunity 39(6): 1121-1131. (Corresponding author)
    S. and Sirianni, A., 22 Jan. 2014. Highlight in the Annual Report 2013 of Institut Pasteur.This study shows in vitro and in vivo that intestinal epithelial cells secrete an endogenous danger signal - ATP - as first alert response to bacterial infection, which acts upstream of classical pro-inflammatory mediators and triggers massive inflammation of the bowel. It further showed that the lipid PtdIns5P blocks the channels secreting ATP. These discoveries were made studying the immune evasion strategies of the pathogen Shigella flexneri. This work bridges the molecular mechanism regulating sterile inflammation (tissue damage, autoimmune diseases) and inflammation during infection. It identifies the extracellular ATP-PtdIns5P axis as potential target for therapy and anti-inflammatory drugs.
    Highlight in the Annual Report 2013 of Institut Pasteur
    Digested in: (2013) Un cible de choix pour le développement d’anti-inflammatoires. La Gazette du Laboratoire, 192.
    Recommendation in: Mostowy, S. and Sirianni, A., 22 Jan. 2014. F1000Prime; DOI: 10.3410/f.718206961. 793489775. F1000Prime.com/ 718206961#eval793489775
    Digested in: (2014) L’ATP joue sur l’immunité. Biofutur, 351, 12.
    Featured article of the Society for Mucosal Immunology, month of April 2014. http://www.socmucimm.org/a-shigella-effector-dampens-inflammation/
  7. Teo, I., Toms, S. M., Marteyn, B., Barata, T. S., Simpson, P., Johnston, K. A., Schnupf, P., Puhar, A., Bell, T., Tang, C., Zloh, M., Matthews, S., Rendle, P. M., Sansonetti, P. J. and Shaunak, S. (2012). Preventing acute gut wall damage in infectious diarrhoeas with glycosylated dendrimers. EMBO Mol Med 4(9): 866-881.
    Comment in: Kelleher, D. (2012). Dendrimers branch out to support mucosal integrity. EMBO Mol. Med., 4(9), 860-2.
  8. Tran, S. L., Puhar, A., Ngo-Camus, M. and Ramarao, N. (2011). Trypan blue dye enters viable cells incubated with the pore-forming toxin HlyII of Bacillus cereus. PLoS One 6(9): e22876.
  9. Konradt, C., Frigimelica, E., Nothelfer, K., Puhar, A., Salgado-Pabon, W., di Bartolo, V., Scott-Algara, D., Rodrigues, C. D., Sansonetti, P. J. and Phalipon, A. (2011). The Shigella flexneri type three secretion system effector IpgD inhibits T cell migration by manipulating host phosphoinositide metabolism. Cell Host Microbe 9(4): 263-272.
    This is one of the first reports on the manipulation of adaptive immunity by a bacterial pathogen and provides an immunological and molecular explanation to the frequent re-infections observed in patients suffering from shigellosis.
    Comment in: Telford, J.L. and Baldari, C.T. (2011) Shigella targets T cells. Cell Host Microbe 9, 253-254.
    Recommendation in: Yu, J. and Jeong, K., 24 May 2011. F1000Prime; DOI: 10.3410/f.10703956.1159. 11592045. F1000Prime.com/10703956#eval 11592054
    Recommendation in: Koronakis, V. and Hume, P., 20 June 2011. F1000 Prime; DOI: 10.3410/f.10703956. 12119054. F1000Prime.com/10703956# eval12119054
  10. Tran, S. L., Guillemet, E., Ngo-Camus, M., Clybouw, C., Puhar, A., Moris, A., Gohar, M., Lereclus, D. and Ramarao, N. (2011). Haemolysin II is a Bacillus cereus virulence factor that induces apoptosis of macrophages. Cell Microbiol 13(1): 92-108.
  11. Puhar, A., Dal Molin, F., Horvath, S., Ladant, D. and Montecucco, C. (2008). Anthrax edema toxin modulates PKA- and CREB-dependent signaling in two phases. PLoS One 3(10): e3564. (Corresponding author)
    This study reveals that anthrax oedema toxin acts on target cells in two distinct phases. Initially, it induces PKA- and CREB-dependent transcription in T cells, but in a second stage it blocks cAMP-dependent signalling such as T cell receptor activation, making the cells unresponsive to immune activation.
  12. Dal Molin, F., Zornetta, I., Puhar, A., Tonello, F., Zaccolo, M. and Montecucco, C. (2008). cAMP imaging of cells treated with pertussis toxin, cholera toxin, and anthrax edema toxin. Biochem Biophys Res Commun 376(2): 429-433.
  13. Lin, P. C., Puhar, A. and Steuber, J. (2008). NADH oxidation drives respiratory Na+ transport in mitochondria from Yarrowia lipolytica. Arch Microbiol 190(4): 471-480.
  14. Puhar, A. and Montecucco, C. (2007). Where and how do anthrax toxins exit endosomes to intoxicate host cells? Trends Microbiol 15(11): 477-482. (Corresponding author)
  15. Genisset, C.*, Puhar, A.*, Calore, F., de Bernard, M., Dell'Antone, P. and Montecucco, C. (2007). The concerted action of the Helicobacter pylori cytotoxin VacA and of the v-ATPase proton pump induces swelling of isolated endosomes. Cell Microbiol 9(6): 1481-1490. (*Equal contribution)
    Using a reconstituted in vitro system, this study identifies the bacterial and mammalian components that are necessary to induce endosomal vacuolisation during intoxication with the main virulence factor of Helicobater pylori, which induce stomach cancer.
  16. Lin, P. C.*, Puhar, A.*, Turk, K., Piligkos, S., Bill, E., Neese, F. and Steuber, J. (2005). A vertebrate-type ferredoxin domain in the Na+-translocating NADH dehydrogenase from Vibrio cholerae. J Biol Chem 280(24): 22560-22563. (*Equal contribution)
  17. Puhar, A., Johnson, E. A., Rossetto, O. and Montecucco, C. (2004). Comparison of the pH-induced conformational change of different clostridial neurotoxins. Biochem Biophys Res Commun 319(1): 66-71.
  18. Turk, K., Puhar, A., Neese, F., Bill, E., Fritz, G. and Steuber, J. (2004). NADH oxidation by the Na+-translocating NADH:quinone oxidoreductase from Vibrio cholerae: functional role of the NqrF subunit. J Biol Chem 279(20): 21349-21355.

Book chapters

  1. Sansonetti, P. J. and Puhar, A. (2010). Overview of bacterial pathogens. In: Kaufmann, S. H. E., Rouse, B. T. and Sacks, D. L. (eds). The Immune Response to Infection. ASM Press.
  2. Türk, K., Puhar, A., Dimroth, P. and Steuber, J. (2002). Spectroscopic Properties of NqrF, the Electron Input Subunit of the Na+-translocating NADH:Quinone Oxidoreductase: a FAD–Fe/S–Protein. In: Perham, S. C. R. and Scrutton, N. (eds). Flavins and Flavoproteins. Agency for Scientific Publication, 667- 672.

Protocols by Andrea Puhar
  1. Induction of Connexin-hemichannel Opening
  2. Dye-uptake Experiment through Connexin Hemichannels