Linked Life Data

7580296

Source:http://linkedlifedata.com/resource/pubmed/id/7580296

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1995-11-28
pubmed:abstractText
We examined the role of lipopolysaccharide (LPS) on the pulmonary inflammatory process in mice, including the release of interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) by macrophages, and investigated the mechanism of action of azelastine (AZ) on the release of these two cytokines. Intratracheal instillation of 1.0 microgram/ml LPS into BALB/c mice caused a significant increase in both IL-1 beta and TNF-alpha in aqueous lung extracts. These changes were modified, under control conditions, by a single dose of 0.05 mg/kg of AZ administered 1 and 11 h after LPS infusion. Intratracheal instillation of LPS also caused a significant increase in bronchial hyperresponsiveness to methacholine (Mch). AZ significantly inhibited Mch responsiveness in LPS-infused mice compared with nontreated control mice. Our results suggested that intratracheal instillation of LPS induces the secretion of macrophage cytokines in the airways of mice, accounting, at least partly, for LPS-induced airway hyperresponsiveness. Our results also indicate that the attenuating effect of AZ on LPS-induced airway hyperresponsiveness could be explained by its inhibitory effect on macrophage cytokine production.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1018-2438
pubmed:author
pubmed:issnType
Print
pubmed:volume
108
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
292-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Effect of azelastine on endotoxin-induced airway hyperresponsiveness in mice.
pubmed:affiliation
First Department of Internal Medicine, School of Medicine, Showa University, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't