AI Article Synopsis
- - The study investigates the protective effects of OprF, a protein from Pseudomonas aeruginosa, in enhancing immune response using mouse dendritic cells (DCs) through both native and recombinant forms of the protein.
- - Both forms of OprF successfully stimulated dendritic cells in the lab, leading to increased cytokine production and costimulatory molecule expression.
- - When these energized DCs were transferred into mice, they provided significant protection against P. aeruginosa infections and related inflammation, showcasing the potential for using DCs in vaccine strategies against such infections.
Article Abstract
Background: 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.
Results: 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.
Conclusions: This study highlights the pivotal contribution of DCs to vaccine-induced protection against P. aeruginosa infection and associated inflammation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820439 | PMC |
| http://dx.doi.org/10.1186/1471-2180-10-9 | DOI Listing |
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