Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-8-17
pubmed:abstractText
Polymorphonuclear leukocytes (PMNL) accumulate in joint fluid in inflammatory arthritides. We investigated the molecular mechanisms required for PMNL migration through a barrier of human synovial fibroblasts (HSF) grown on microporous filters, as a model of PMNL migration through synovial connective tissue and compared this process with PMNL migration through human dermal fibroblast (HDF) barriers and through human umbilical vein endothelium (HUVE). A small amount of PMNL migration occurred spontaneously only through the synovial fibroblast/filter unit (6-10%). Migration markedly increased through all cell monolayers when the chemotactic factors C5a, IL-8, or zymosan-activated plasma (containing C5adesArg) were added to form a chemotactic gradient. The migration induced by C5a, IL-8, or C5adesArg across HSF was partially inhibited (25-76% depending on stimulus) by mAb to CD18 (beta 2 integrin). The CD18-independent migration induced by IL-8 or C5adesArg was almost completely inhibited by mAbs to beta 1 integrin, but with C5a, inhibition by mAb to beta 1 integrin was only partial (40-50%). Inhibition by mAb to beta 1 integrin required treatment of the PMNL, but not the HSF and was only observed when the function of CD11/CD18 on PMNL was also blocked by a mAb. Treatment of PMNL with mAb to alpha 5 (VLA-5) plus alpha 6 (VLA-6) in combination, was required to inhibit CD18-independent migration through HSF to the degree observed with mAb to beta 1 integrin. There was no qualitative difference in the mechanisms utilized by PMNL for migration through HSF or HDF in response to chemotactic factors. In contrast, PMNL migration across HUVE was almost completely CD18-dependent (85%) with no role for beta 1 integrins. The results suggest that (a) PMNL migration through HSF in response to chemotactic factors utilizes both CD11/CD18 and beta 1 (CD29) integrins; (b) the VLA-5 and VLA-6 members of beta 1 integrins are involved in mediating migration; and (c) PMNL utilize similar mechanisms for migration through HSF and HDF, which are distinct from migration through HUVE.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0008-8749
pubmed:author
pubmed:issnType
Print
pubmed:volume
163
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
178-86
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:7541723-Antibodies, Monoclonal, pubmed-meshheading:7541723-Antigens, CD, pubmed-meshheading:7541723-Antigens, CD11, pubmed-meshheading:7541723-Antigens, CD18, pubmed-meshheading:7541723-Antigens, CD29, pubmed-meshheading:7541723-Cell Movement, pubmed-meshheading:7541723-Cells, Cultured, pubmed-meshheading:7541723-Chemotactic Factors, pubmed-meshheading:7541723-Complement C5a, pubmed-meshheading:7541723-Endothelium, Vascular, pubmed-meshheading:7541723-Fibroblasts, pubmed-meshheading:7541723-Humans, pubmed-meshheading:7541723-Integrins, pubmed-meshheading:7541723-Neutrophils, pubmed-meshheading:7541723-Receptors, Fibronectin, pubmed-meshheading:7541723-Receptors, Very Late Antigen, pubmed-meshheading:7541723-Skin, pubmed-meshheading:7541723-Synovial Membrane, pubmed-meshheading:7541723-Umbilical Veins
pubmed:year
1995
pubmed:articleTitle
Migration of human polymorphonuclear leukocytes through a synovial fibroblast barrier is mediated by both beta 2 (CD11/CD18) integrins and the beta 1 (CD29) integrins VLA-5 and VLA-6.
pubmed:affiliation
Department of Pediatrics, Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia, Canada.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't