PubMed Health⌕ Search

PubMed · 7691452

Soluble E-selectin in arthritis.

Abstract

Cellular adhesion molecules, such as E-selectin, function to recruit leukocytes into inflammatory lesions. Recently, a soluble form of this adhesion molecule, sE-selectin, has been described. In this study we determined soluble E-selectin (sE-selectin) in synovial fluid (SF) and blood samples from patients with rheumatoid arthritis (RA) and other inflammatory disorders and correlated sE-selectin levels with clinical parameters of disease activity. SF, blood, and cells isolated from RA SFs and synovial tissues (STs) were examined from 76 patients. In addition, normal plasma as well as supernatants from cultured human umbilical vein endothelial cells (HUVECs) were obtained. sE-selectin levels were assayed in these fluids and cell supernatants by an enzyme-linked immunoabsorbant (ELISA) assay. SFs from patients with RA had significantly higher sE-selectin levels than did those from osteoarthritis (OA) SFs (P < 0.05). SF sE-selectin levels were correlated with SF leukocyte counts. HUVECs, or RA ST cells enriched in endothelial cells, produced sE-selectin. Neutrophils isolated from RA SFs did not release sE-selectin. SF soluble intercellular adhesion molecule-1 levels correlated positively with sE-selectin levels. We conclude that sE-selectin levels are increased in SFs from RA compared to those from OA. Endothelial cells derived from umbilical vein or from RA STs release sE-selectin. Thus, sE-selectin may be important in the migration of inflammatory leukocytes into diseased RA STs and SFs.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A E Koch, W Turkiewicz, L A Harlow, R M Pope. 1993. Soluble E-selectin in arthritis.. https://doi.org/10.1006/clin.1993.1146

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Interleukin-18 genetics and inflammatory disease susceptibility.

IL18 was mapped to 11q22.2-22.3 in 1998. Owing to interleukin (IL)-18's important and novel role in immunomodulation, the gene itself has been subject to scrutiny, with the aim of discovering variants that may impact on disease susceptibility and/or progression. Despite being sequenced numerous times in different populations, no non-synonymous variants have been found. However, a number of polymorphisms within the proximal promoter have been verified that may interfere with transcription-factor-binding sites. Much of the subsequent association analyses have centred on these variants, but have yielded no consistent results, despite numerous different study populations being genotyped. IL18 has recently been resequenced in its entirety, enabling the tagging-single-nucleotide polymorphism (tSNP) methodology to be adopted. This approach has yielded interesting results, with genetic variation being shown to affect protein levels, and risk. This review aims to compile and reflect on the association data of interest published to date, with a focus on the diseases related to aberrant inflammatory control.

Arthritis↗