Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2 Pt 1
pubmed:dateCreated
1999-9-23
pubmed:abstractText
Enteric nematode infections lead to increased interleukin (IL)-5 expression, eosinophilic inflammation, and intestinal smooth muscle hypercontractility. Although eosinophils release inflammatory mediators that cause smooth muscle contraction, the role of IL-5 and eosinophils in enteric smooth muscle hypercontractility is unclear. IL-5-deficient mice and their wild-type controls were infected with the nematode Trichinella spiralis. Intestinal parasites and eosinophils were counted, and jejunal longitudinal muscle contractility was assessed. During infection, IL-5 gene expression increased significantly in wild-type mice and was accompanied by significant intestinal eosinophilia in wild-type but not IL-5-deficient mice. Although both strains developed increased muscle contractility during infection, contraction was significantly less in the IL-5-deficient mice at days 16 and 21 postinfection. In addition, parasite expulsion was transiently delayed at day 16 in IL-5-deficient mice. Thus, in the nematode-infected mouse, IL-5 appears essential for intestinal eosinophilia and contributes to, but is not essential for, the development of muscle hypercontractility. IL-5 also appears to play a minor role in expelling a primary T. spiralis infection from the gut.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
277
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
G400-8
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
IL-5 contributes to worm expulsion and muscle hypercontractility in a primary T. spiralis infection.
pubmed:affiliation
Intestinal Diseases Research Program, Department of Medicine, McMaster University, Hamilton, Ontario, Canada L8N 3Z5.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't