Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2001-5-8
pubmed:abstractText
Glucocorticoids can dampen inflammatory responses by inhibiting neutrophil recruitment to tissue sites. The detailed mechanism by which glucocorticoids exert this affect on neutrophils is unknown. L-selectin is a leukocyte cell surface receptor that is implicated in several steps of neutrophil recruitment. Recently, several studies have shown that systemic treatment of animals and humans with glucocorticoids induces decreased L-selectin expression on neutrophils, suggesting one mechanism by which inflammation may be negatively regulated. However, when neutrophils are treated in vitro with glucocorticoids, no effect on L-selectin expression is observed. Thus, the existence of an additional mediator is plausible. In this study, we investigate whether annexin 1 (ANX1), a recognized second messenger of glucocorticoids, could be such a mediator. We show that ANX1 induces a dose- and time-dependent decrease in L-selectin expression on both peripheral blood neutrophils and monocytes but has no effect on lymphocytes. The loss of L-selectin from neutrophils is due to shedding that is mediated by a cell surface metalloprotease ("sheddase"). Using cell shape and a beta(2) integrin activation epitope, we show that the ANX1-induced shedding of L-selectin appears to occur without overt cell activation. These data may provide the basis for further understanding of mechanisms involved in the down-regulation of inflammatory responses.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
166
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6294-300
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11342653-Animals, pubmed-meshheading:11342653-Annexins, pubmed-meshheading:11342653-Cattle, pubmed-meshheading:11342653-Cell Size, pubmed-meshheading:11342653-Dexamethasone, pubmed-meshheading:11342653-Dose-Response Relationship, Immunologic, pubmed-meshheading:11342653-Down-Regulation, pubmed-meshheading:11342653-Flow Cytometry, pubmed-meshheading:11342653-Humans, pubmed-meshheading:11342653-L-Selectin, pubmed-meshheading:11342653-Leukocytes, pubmed-meshheading:11342653-Metalloendopeptidases, pubmed-meshheading:11342653-Myeloid Cells, pubmed-meshheading:11342653-N-Formylmethionine Leucyl-Phenylalanine, pubmed-meshheading:11342653-Neutrophil Activation, pubmed-meshheading:11342653-Receptors, Formyl Peptide, pubmed-meshheading:11342653-Receptors, Immunologic, pubmed-meshheading:11342653-Receptors, Peptide, pubmed-meshheading:11342653-Tetradecanoylphorbol Acetate
pubmed:year
2001
pubmed:articleTitle
A potential role for annexin 1 as a physiologic mediator of glucocorticoid-induced L-selectin shedding from myeloid cells.
pubmed:affiliation
Department of Anatomy, Program in Immunology and Cardiovascular Research Institute, University of California, San Francisco, CA 94143, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't