Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2003-12-4
pubmed:abstractText
The purpose of this study was to investigate the influence of pranlukast on eosinophilic inflammation and cytokine production in human nasal mucosa. Twelve patients were treated with pranlukast, and samples were obtained from the nasal mucosa of the inferior turbinate. With respect to cell infiltration, a significant decrease was observed in the percentage of inflammatory cells (secreted eosinophil cationic protein [EG2] and neutrophil elastase) after treatment. The levels of cytokines and chemical mediators (interleukin [IL]-4, IL-5, RANTES [regulated on activation, normal T cell expressed and secreted], cysteinyl leukotrienes, IL-1beta, tumor necrosis factor-alpha, and IL-8) assessed by enzyme-linked immunosorbent assay and enzyme immunoassay were significantly decreased. These results indicate that pranlukast decreased the levels of a majority of the cytokines in nasal mucosa, leading to improvement in subjective nasal symptoms. Furthermore, these results support the hypothesis that pranlukast exerts its therapeutic action primarily by blocking the leukotriene receptors on eosinophils.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0003-4894
pubmed:author
pubmed:issnType
Print
pubmed:volume
112
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
955-61
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Leukotriene receptor antagonist pranlukast suppresses eosinophil infiltration and cytokine production in human nasal mucosa of perennial allergic rhinitis.
pubmed:affiliation
Department of Otorhinolaryngology-Head and Neck Surgery, Division of Clinical Medical Programs for Applied Biomedicine, Graduate School of Biomedical Science, Hiroshima University, Hiroshima, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't