Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1996-10-25
pubmed:abstractText
Chronic immune responses and inflammatory reactions in rheumatoid arthritis (RA) often cause severe destruction of cartilage and bone, but its mechanism is still a matter of controversy. We reported that interleukin-6 (IL-6) alone does not induce osteoclast formation, but soluble interleukin-6 receptors (sIL-6R) triggered the formation in the presence of IL-6 in cocultures of murine osteoblastic cells and bone marrow cells. In this study, we examined the involvement of sIL-6R and IL-6 in joint destruction in patients with RA. Although the frequency of patients having osteoclast-like multinucleated cells in synovium derived from the knee joint was not significantly different between RA (65%) and osteoarthritis (OA) patients (43%), the number of osteoclast-like cells found in the synovium was greater in the former than in the latter. Multinucleated cells obtained from RA synovium expressed the osteoclast-specific phenotype such as tartrate-resistant acid phosphatase, carbonic anhydrase II, vacuolar proton-ATPase and vitronectin receptors at similar levels to those from a human giant cell tumor of bone. The concentration of both IL-6 and sIL-6R was significantly higher in the synovial fluids from patients with RA than with OA. The concentration of IL-6 and sIL-6R correlated well with the roentgenologic grades of joint destruction. Dose-response curves for human IL-6 and human sIL-6R in inducing osteoclast-like cell formation in cocultures indicated that the RA synovial fluids contained sufficient IL-6 and sIL-6R to induce osteoclastogenesis. When synovial fluids from RA and OA patients were added to the cocultures, some of the RA synovial fluids containing high levels of IL-6 and sIL-6R stimulated osteoclast-like cell formation, which was strikingly inhibited by adding anti-IL-6R antibody simultaneously. These results suggest that IL-6 in the RA synovial fluids is at least in part responsible for joint destruction in the presence of sIL-6R through osteoclastogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0884-0431
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
88-95
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8770701-Acid Phosphatase, pubmed-meshheading:8770701-Adult, pubmed-meshheading:8770701-Aged, pubmed-meshheading:8770701-Aged, 80 and over, pubmed-meshheading:8770701-Animals, pubmed-meshheading:8770701-Antigens, CD, pubmed-meshheading:8770701-Arthritis, Rheumatoid, pubmed-meshheading:8770701-Cells, Cultured, pubmed-meshheading:8770701-Female, pubmed-meshheading:8770701-Humans, pubmed-meshheading:8770701-Interleukin-6, pubmed-meshheading:8770701-Male, pubmed-meshheading:8770701-Mice, pubmed-meshheading:8770701-Middle Aged, pubmed-meshheading:8770701-Osteoarthritis, pubmed-meshheading:8770701-Osteoblasts, pubmed-meshheading:8770701-Osteoclasts, pubmed-meshheading:8770701-Phenotype, pubmed-meshheading:8770701-Receptors, Interleukin, pubmed-meshheading:8770701-Receptors, Interleukin-6, pubmed-meshheading:8770701-Solubility, pubmed-meshheading:8770701-Synovial Fluid, pubmed-meshheading:8770701-Synovial Membrane
pubmed:year
1996
pubmed:articleTitle
Interleukin-6 and soluble interleukin-6 receptors in the synovial fluids from rheumatoid arthritis patients are responsible for osteoclast-like cell formation.
pubmed:affiliation
Institute of Rheumatology, Tokyo Women's Medical College, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't