Source:http://linkedlifedata.com/resource/pubmed/id/12760968
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
|
pubmed:dateCreated |
2003-5-22
|
pubmed:abstractText |
In patients with asthma, eosinophils are primed and massively infiltrate lung tissues and migrate across epithelia into airways. Using blocking monoclonal antibodies, we found that eosinophil transmigration across a lung epithelial cell monolayer depended on the functions of alphaMbeta2 integrin CD11b/CD18. To study the role of Ca2+ in eosinophil priming and transepithelial migration, we treated eosinophils with eotaxin or thapsigargin (TG), reagents that increase cytoplasmic free Ca2+ concentrations by receptor- or nonreceptor-mediated mechanisms, respectively. Pretreatment of eosinophils with TG enhanced CD11b/CD18-dependent transmigration across lung epithelium. Within minutes, TG time- and dose-dependently upregulated the expression of CD11b/CD18 but did not upregulate the expression of alphaL (CD11a) or beta1 (CD29) integrin. The upregulation of CD11b/CD18 expression by eotaxin or TG was prevented when Ca2+ entry was blocked. The priming of eosinophil transmigration by TG was also abrogated by the blockade of Ca2+ entry. Our results indicate that induction of Ca2+ entry by the depletion of Ca2+ from intracellular stores upregulates CD11b/CD18 expression on eosinophils and primes eosinophil transmigration across lung epithelium. Both responses are therefore elicited by extracellular Ca2+. We suggest that, as an important priming signal for human eosinophil functional responses, store-operated Ca2+ entry may be one of the underlying mechanisms of eosinophilic inflammation in asthma.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD11b,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD18,
http://linkedlifedata.com/resource/pubmed/chemical/CCL11 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL11,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CC,
http://linkedlifedata.com/resource/pubmed/chemical/Chemotactic Factors, Eosinophil,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Lanthanum,
http://linkedlifedata.com/resource/pubmed/chemical/Thapsigargin
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jun
|
pubmed:issn |
1044-1549
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
28
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
713-21
|
pubmed:dateRevised |
2007-11-15
|
pubmed:meshHeading |
pubmed-meshheading:12760968-Antigens, CD11b,
pubmed-meshheading:12760968-Antigens, CD18,
pubmed-meshheading:12760968-Calcium,
pubmed-meshheading:12760968-Cell Movement,
pubmed-meshheading:12760968-Cells, Cultured,
pubmed-meshheading:12760968-Chemokine CCL11,
pubmed-meshheading:12760968-Chemokines, CC,
pubmed-meshheading:12760968-Chemotactic Factors, Eosinophil,
pubmed-meshheading:12760968-Chemotaxis, Leukocyte,
pubmed-meshheading:12760968-Enzyme Inhibitors,
pubmed-meshheading:12760968-Eosinophils,
pubmed-meshheading:12760968-Epithelial Cells,
pubmed-meshheading:12760968-Extracellular Space,
pubmed-meshheading:12760968-Humans,
pubmed-meshheading:12760968-Lanthanum,
pubmed-meshheading:12760968-Lung,
pubmed-meshheading:12760968-Thapsigargin,
pubmed-meshheading:12760968-Up-Regulation
|
pubmed:year |
2003
|
pubmed:articleTitle |
Priming of eosinophil migration across lung epithelial cell monolayers and upregulation of CD11b/CD18 are elicited by extracellular Ca2+.
|
pubmed:affiliation |
Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden. lixliu@ucalgary.ca
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|