My research focuses onthe study of pathogen-host interaction in the context of respiratoryinfections. During the past few years, I have studied how the respiratorypathogen Pseudomonas aeruginosa interacts with airway epithelial cells. While I initially focused on themolecular mechanisms underlying this interaction, I have also been interestedin understanding the implication of this binding on the host immune system. Inmy recent work, I am using a broader approach for the understanding ofpathogen-host interaction. I am currently working on molecular tools to label awide range of bacteria with fluorescent markers and study the expression ofvirulence factors in vivo.

M. Barbier, J.P. Owings, I.Martínez-Ramos, R. Gomila, F.H. Damron, J. Blázquez, J.B. Goldbergand S. Albertí. Lysine trimethylation of EF-Tumimics platelet-activating factor to initiate Pseudomonasaeruginosa pneumonia. mBio, vol. 4 no. 3, e00207-13.

F.H. Damron, E.S. McKenney, M.Barbier, G. Liechti, H. Schweiser and J. B. Goldberg. Construction ofmobilizable mini-Tn7 vectorsfor bioluminescent detection of gram-negative bacteria and single-copy promoterlux reporter analysis. AEM, 2013 Jul;79(13):4149-53. 

M. Barbier, I.Martínez-Ramos, P. Townsend, and S. Albertí. Surfactant protein A blocksrecognition ofPseudomonas aeruginosa byCKAP4/P63 on airway epithelial cells. JID. 2012 Dec; 206(11): 1753-1762. 

M.Barbier, A. Agustí, and S. Albertí. Fluticasone propionate reduces bacterial airway epithelialinvasion.Eur Respir J. 2008; 32: 1283–1288.

M. Barbier, A. Oliver, J. Rao, S.L. Hanna, J.B. Goldberg, and S.Albertí. Novel Phosphorylcholine-Containing Protein of Pseudomonas aeruginosa Chronic Infection Isolates Interactswith Airway Epithelial Cells. JID.2008; 197:465-473.