Linked Life Data

21471450

Source:http://linkedlifedata.com/resource/pubmed/id/21471450

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2011-5-4
pubmed:abstractText
Allergic airway inflammation is generally considered a Th2-type immune response. Recent studies, however, demonstrated that Th17-type immune responses also play important roles in this process, especially in the pathogenesis of neutrophilic airway inflammation, a hallmark of severe asthma. We previously reported that dendritic cells release dopamine to naive CD4(+) T cells in Ag-specific cell-cell interaction, in turn inducing Th17 differentiation through dopamine D1-like receptor (D1-like-R). D1-like-R antagonist attenuates Th17-mediated diseases such as experimental autoimmune encephalomyelitis and autoimmune diabetes. However, the effect of antagonizing D1-like-R on Th17-mediated airway inflammation has yet to be studied. In this study, we examined whether D1-like-R antagonist suppresses OVA-induced neutrophilic airway inflammation in OVA TCR-transgenic DO11.10 mice and then elucidated the mechanism of action. DO11.10 mice were nebulized with OVA or PBS, and some mice received D1-like-R antagonist orally before OVA nebulization. D1-like-R antagonist significantly suppressed OVA-induced neutrophilic airway inflammation in DO11.10 mice. It also inhibited the production of IL-17 and infiltration of Th17 cells in the lung. Further, D1-like-R antagonist suppressed the production of IL-23 by lung CD11c(+) APCs. In contrast, D1-like-R antagonist did not increase Foxp3(+) regulatory T cells in the lung. D1-like-R antagonist neither suppressed nonspecific LPS-induced neutrophilic airway inflammation nor OVA-induced eosinophilic airway inflammation. These results indicate that D1-like-R antagonist could suppress Th17-mediated neutrophilic airway inflammation, raising the possibility that antagonizing D1-like-R serves as a promising new strategy for treating neutrophil-dominant severe asthma.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
186
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5975-82
pubmed:meshHeading
pubmed-meshheading:21471450-Animals, pubmed-meshheading:21471450-Benzazepines, pubmed-meshheading:21471450-Bronchoalveolar Lavage Fluid, pubmed-meshheading:21471450-Dopamine, pubmed-meshheading:21471450-Female, pubmed-meshheading:21471450-Forkhead Transcription Factors, pubmed-meshheading:21471450-Inflammation, pubmed-meshheading:21471450-Interleukin-23, pubmed-meshheading:21471450-Lipopolysaccharides, pubmed-meshheading:21471450-Mice, pubmed-meshheading:21471450-Mice, Inbred BALB C, pubmed-meshheading:21471450-Mice, Transgenic, pubmed-meshheading:21471450-Neutrophils, pubmed-meshheading:21471450-Ovalbumin, pubmed-meshheading:21471450-Receptors, Dopamine D1, pubmed-meshheading:21471450-Respiratory Hypersensitivity, pubmed-meshheading:21471450-T-Lymphocytes, Regulatory, pubmed-meshheading:21471450-Th17 Cells
pubmed:year
2011
pubmed:articleTitle
Dopamine D1-like receptor antagonist attenuates Th17-mediated immune response and ovalbumin antigen-induced neutrophilic airway inflammation.
pubmed:affiliation
Department of Respiratory Medicine, Saitama Medical University, Saitama 350-0495, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't