Linked Life Data

9863651

Source:http://linkedlifedata.com/resource/pubmed/id/9863651

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1999-3-25
pubmed:abstractText
Tissue eosinophilia is a hallmark of allergic and parasitic diseases. Priming mechanisms may play an important role in mediating the process of eosinophil accumulation in these conditions. We have previously shown that blockade of tumour necrosis factor alpha (TNFalpha) inhibited the capacity of lipopolysaccharide to prime skin sites for chemoattractant-induced eosinophil recruitment. The present study was carried out to investigate the capacity of TNFalpha to prime an inflammatory site for enhanced eosinophil accumulation. Initial experiments investigated the capacity of TNFalpha itself to induce eosinophil accumulation. Intradermal injection of murine TNFalpha (10-300 ng per site) in the guinea-pig induced significant accumulation of 111In-eosinophils. Kinetic studies showed the response to be delayed in onset and inhibited by cycloheximide, consistent with a dependency on protein synthesis. Trafficking of 111In-eosinophils to sites treated for 2 h with TNFalpha (10-100 ng per site) was inhibited by monoclonal antibodies (mAbs) against beta2 or alpha4 integrins. Intradermal injection of a low dose (3 ng) of TNFalpha (which by itself had no significant effect on eosinophil trafficking) prior to chemoattractants or antigen in sensitized skin sites, induced significant priming of eosinophil accumulation. Recruitment of both 111In-eosinophils and endogenous eosinophils was enhanced. Trafficking to TNFalpha-primed responses was dependent on protein synthesis and beta2 integrins. In contrast, the alpha4 integrin mAb failed to inhibit the TNFalpha primed response. Thus, TNFalpha can induce and also prime eosinophil recruitment in guinea-pig skin. Our results provide further evidence that this cytokine may be an important mediator of allergic- or parasite-induced eosinophilic inflammation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0007-1188
pubmed:author
pubmed:issnType
Print
pubmed:volume
125
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1228-35
pubmed:dateRevised
2008-11-20
pubmed:meshHeading
pubmed-meshheading:9863651-Animals, pubmed-meshheading:9863651-Antibodies, Monoclonal, pubmed-meshheading:9863651-Antigens, CD18, pubmed-meshheading:9863651-Cell Movement, pubmed-meshheading:9863651-Cycloheximide, pubmed-meshheading:9863651-Dermatitis, pubmed-meshheading:9863651-Dose-Response Relationship, Drug, pubmed-meshheading:9863651-Eosinophils, pubmed-meshheading:9863651-Female, pubmed-meshheading:9863651-Guinea Pigs, pubmed-meshheading:9863651-Horses, pubmed-meshheading:9863651-Humans, pubmed-meshheading:9863651-Indium Radioisotopes, pubmed-meshheading:9863651-Injections, Intradermal, pubmed-meshheading:9863651-Integrin alpha4beta1, pubmed-meshheading:9863651-Integrins, pubmed-meshheading:9863651-Male, pubmed-meshheading:9863651-Mice, pubmed-meshheading:9863651-Protein Synthesis Inhibitors, pubmed-meshheading:9863651-Receptors, Lymphocyte Homing, pubmed-meshheading:9863651-Skin, pubmed-meshheading:9863651-Tumor Necrosis Factor-alpha
pubmed:year
1998
pubmed:articleTitle
Priming and induction of eosinophil trafficking in guinea-pig cutaneous inflammation by tumour necrosis factor alpha.
pubmed:affiliation
Applied Pharmacology, Imperial College School of Medicine at the National Heart and Lung Institute, London.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't