Linked Life Data

17641297

Source:http://linkedlifedata.com/resource/pubmed/id/17641297

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-12-13
pubmed:abstractText
Particle-mediated epidermal delivery (PMED) of allergen genes efficiently prevents systemic sensitization and suppresses specific immunoglobulin E synthesis. We investigated in a mouse model of allergic airway disease the effect of PMED on the elicitation of local inflammatory reactions in the lung. BALB/c mice were biolistically transfected with plasmids encoding beta-galactosidase (betaGal) as model allergen under control of the DC-targeting fascin promoter and the ubiquitously active cytomegalovirus promoter, respectively. Mice were challenged intranasally with betaGal-protein with or without intermediate sensitization with betaGal adsorbed to aluminiumhydroxide. Subsequently, local cytokine production and recruitment of IFN-gamma-producing CD8(+) effector T cells into the airways were determined, and inflammatory parameters such as cellular infiltration in the bronchoalveolar lavage (BAL) and airway hyperresponsiveness (AHR) were measured. PMED of betaGal-encoding plasmids before sensitization significantly reduced frequencies of eosinophils in the BAL and shifted the local T helper (Th) cell response from a distinct Th2 response toward a Th1-biased response. However, AHR triggered by allergen challenge via the airways was not alleviated in vaccinated mice. Most important, we show that PMED using betaGal-encoding DNA without subsequent sensitization recruited Tc1 cells into the lung and caused a Th1-prone local immune response after subsequent intranasal provocation, accompanied by neutrophilic infiltration into the airways and elicitation of AHR. We conclude that robust Th1/Tc1 immune responses, although highly effective in the counter-regulation of local Th2-mediated pathology, might as well trigger local inflammatory reactions in the lung and provoke the induction of AHR in the mouse model of allergic airway disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1535-4989
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
38
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
38-46
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:17641297-Animals, pubmed-meshheading:17641297-Antibody Formation, pubmed-meshheading:17641297-Bronchoalveolar Lavage Fluid, pubmed-meshheading:17641297-Carrier Proteins, pubmed-meshheading:17641297-Cells, Cultured, pubmed-meshheading:17641297-Cytomegalovirus, pubmed-meshheading:17641297-Dendritic Cells, pubmed-meshheading:17641297-Disease Models, Animal, pubmed-meshheading:17641297-Epidermis, pubmed-meshheading:17641297-Female, pubmed-meshheading:17641297-Gene Transfer Techniques, pubmed-meshheading:17641297-Humans, pubmed-meshheading:17641297-Immunoglobulin E, pubmed-meshheading:17641297-Inflammation, pubmed-meshheading:17641297-Interferon-gamma, pubmed-meshheading:17641297-Lung, pubmed-meshheading:17641297-Mice, pubmed-meshheading:17641297-Mice, Inbred BALB C, pubmed-meshheading:17641297-Microfilament Proteins, pubmed-meshheading:17641297-Neutrophil Infiltration, pubmed-meshheading:17641297-Promoter Regions, Genetic, pubmed-meshheading:17641297-Respiratory Hypersensitivity, pubmed-meshheading:17641297-T-Lymphocytes, Cytotoxic, pubmed-meshheading:17641297-Th1 Cells, pubmed-meshheading:17641297-Th2 Cells, pubmed-meshheading:17641297-beta-Galactosidase
pubmed:year
2008
pubmed:articleTitle
Divergent effects of biolistic gene transfer in a mouse model of allergic airway inflammation.
pubmed:affiliation
Clinical Research Unit Allergology, Department of Dermatology, Johannes Gutenberg-University Mainz, Obere Zahlbacher Str. 63, D-55131 Mainz, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't