Linked Life Data

9070605

Source:http://linkedlifedata.com/resource/pubmed/id/9070605

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1997-4-14
pubmed:abstractText
Interleukin (IL)-5 is thought to play an important role in asthmatic bronchial mucosal inflammation and is a potential therapeutic target. To investigate the effect of IL-5 on the infiltration of eosinophils in airway in vivo, we compared eosinophil counts and their activation status in airways without and after the topical instillation of recombinant human IL-5. Eight subjects with mild atopic asthma underwent initial bronchoscopy during which control bronchoalveolar lavage (BAL) fluid as well as bronchial mucosa were obtained, and at the same time, normal saline and IL-5 were administered to two sublobar segments separately. The second bronchoscopy were carried out and samples from challenged sites were taken 24 h later. It was found that the total eosinophils (BMK-13+ cells) and the activated eosinophils (EG2+ cells) in bronchial mucosa, the eosinophil numbers in BAL fluid, as well as eosinophil cationic protein (ECP) in BAL fluid from saline-challenged segments were not different from those in unchallenged segments. However, a significant eosinophilia was observed in bronchial mucosa and BAL fluid from IL-5-challenged sites. Eosinophil activation, as assessed by secretion of ECP, was also increased significantly in bronchial mucosa and BAL fluid. The results strongly suggested that IL-5 is capable of inducing eosinophil infiltration into the asthmatic airways, as well as the activation of infiltrating eosinophils.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1044-1549
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
220-4
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Infiltration of eosinophils into the asthmatic airways caused by interleukin 5.
pubmed:affiliation
Department of Internal Medicine, Guangxi Medical University, Nanning, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't