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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2011-5-20
pubmed:abstractText
Neurotrophins such as nerve growth factor and brain-derived neurotrophic factor have been described to be involved in the pathogenesis of asthma. Neurturin (NTN), another neurotrophin from the glial cell line-derived neurotrophic factor family, was shown to be produced by human immune cells: monocytes, B cells, and T cells. Furthermore, it was previously described that the secretion of inflammatory cytokines was dramatically stimulated in NTN knockout (NTN(-/-)) mice. NTN is structurally similar to TGF-?, a protective cytokine in airway inflammation. This study investigates the implication of NTN in a model of allergic airway inflammation using NTN(-/-) mice. The bronchial inflammatory response of OVA-sensitized NTN(-/-) mice was compared with wild-type mice. Airway inflammation, Th2 cytokines, and airway hyperresponsiveness (AHR) were examined. NTN(-/-) mice showed an increase of OVA-specific serum IgE and a pronounced worsening of inflammatory features. Eosinophil number and IL-4 and IL-5 concentration in the bronchoalveolar lavage fluid and lung tissue were increased. In parallel, Th2 cytokine secretion of lung draining lymph node cells was also augmented when stimulated by OVA in vitro. Furthermore, AHR was markedly enhanced in NTN(-/-) mice after sensitization and challenge when compared with wild-type mice. Administration of NTN before challenge with OVA partially rescues the phenotype of NTN(-/-) mice. These findings provide evidence for a dampening role of NTN on allergic inflammation and AHR in a murine model of asthma.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
186
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6497-504
pubmed:meshHeading
pubmed-meshheading:21508262-Animals, pubmed-meshheading:21508262-Antibodies, pubmed-meshheading:21508262-Asthma, pubmed-meshheading:21508262-Bronchial Hyperreactivity, pubmed-meshheading:21508262-Bronchoalveolar Lavage Fluid, pubmed-meshheading:21508262-Cytokines, pubmed-meshheading:21508262-Eosinophils, pubmed-meshheading:21508262-Flow Cytometry, pubmed-meshheading:21508262-Glial Cell Line-Derived Neurotrophic Factor Receptors, pubmed-meshheading:21508262-Lung, pubmed-meshheading:21508262-Lymph Nodes, pubmed-meshheading:21508262-Mice, pubmed-meshheading:21508262-Mice, Inbred C57BL, pubmed-meshheading:21508262-Mice, Knockout, pubmed-meshheading:21508262-Neurturin, pubmed-meshheading:21508262-Ovalbumin, pubmed-meshheading:21508262-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:21508262-Th2 Cells
pubmed:year
2011
pubmed:articleTitle
Increased Th2 cytokine secretion, eosinophilic airway inflammation, and airway hyperresponsiveness in neurturin-deficient mice.
pubmed:affiliation
Laboratoire d'Immunogénétique et d'Allergologie, Centre de Recherche Public de la Santé, L-1526 Luxembourg, Luxembourg. tatiana.michel@crp-sante.lu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't