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Protection against Pseudomonas aeruginosa lung infection in mice by recombinant OprF-pulsed dendritic cell immunization

Lucia Peluso1, Cristiana de Luca1, Silvia Bozza2, Antonio Leonardi1, Gloria Giovannini2, Alfonso Lavorgna1, Gaetano De Rosa34, Massimo Mascolo3, Loredana Ortega De Luna1, Maria Rosaria Catania1, Luigina Romani2 and Fabio Rossano1*

Author Affiliations

1 Department of Cellular and Molecular Biology and Pathology "L. Califano", University of Naples "Federico II", Via S. Pansini 5, 80131 Naples, Italy

2 Department of Experimental Medicine and Biochemical Sciences, Section of Microbiology, University of Perugia, Via del Giochetto, 06122 Perugia, Italy

3 Department of Biomorphological and Functional Sciences, Section of Pathology, University of Naples "Federico II", Via S. Pansini 5, 80131 Naples, Italy

4 Oncology Referral Center of Basilicata (CROB), Regional Oncology Hospital, Rionero in Vulture, Potenza, Italy

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BMC Microbiology 2010, 10:9  doi:10.1186/1471-2180-10-9

Published: 13 January 2010



The Pseudomonas aeruginosa major constitutive outer membrane porin protein F (OprF) has been shown to be a protective antigen and was previously used to activate an immunological response in a mouse model of lung pneumonia. The purpose of our study was to demonstrate the ability of mouse dendritic cells pulsed with purified or recombinant OprF to protect mice against P. aeruginosa infection and inflammation.

Both native (n-OprF), isolated and purified from PAO1 bacterial strain, and recombinant (histidin-conjugated) OprF (His-OprF), obtained by cloning of the oprF gene into the pET28a expression vector, were used to stimulate dendritic cells in vitro before adoptive transfer into prospective recipient mice with P. aeruginosa pulmonary infection.


Similar to n-OprF, His-OprF activated dendritic cells in vitro, inducing the costimulatory molecule expression as well as cytokine production. Upon adoptive transfer in vivo, porin-pulsed dendritic cells (DCs) induced Th1-mediated resistance to infection and associated inflammatory pathology caused by either the PAO1 strain or a clinically-isolated mucoid strain.


This study highlights the pivotal contribution of DCs to vaccine-induced protection against P. aeruginosa infection and associated inflammation.