INDUCTION OF INTRAARTICULAR TUMOR-NECROSIS-FACTOR DURING ACUTE INFLAMMATORY RESPONSES IN EQUINE ARTHRITIS

Citation
Rc. Billinghurst et al., INDUCTION OF INTRAARTICULAR TUMOR-NECROSIS-FACTOR DURING ACUTE INFLAMMATORY RESPONSES IN EQUINE ARTHRITIS, Equine veterinary journal, 27(3), 1995, pp. 208-216
Citations number
44
Categorie Soggetti
Veterinary Sciences
Journal title
ISSN journal
04251644
Volume
27
Issue
3
Year of publication
1995
Pages
208 - 216
Database
ISI
SICI code
0425-1644(1995)27:3<208:IOITDA>2.0.ZU;2-S
Abstract
Synovial fluid (SF) was collected at 2, 12 and 26 h post racing from 5 Thoroughbred horses (6 joints) with degenerative joint disease. The e ffects of serial arthrocentesis on SF TNF alpha levels were controlled for by testing, in parallel, site- and time-matched samples from clin ically normal horses (i.e. without arthritis). A significant induction in TNF alpha bioactivity was detected in SF from arthritic joints (co mpared to the control joints) over the 26 h following racing. After su btraction of values for the arthrocentesis control SF, TNF alpha and p rotein levels and WBC and mononuclear cell numbers each peaked at 12 h in the SF from the degenerative joints, although there were no statis tically significant correlations between any of these parameters. The presence in the SF of TNF alpha, as well as immunoreactive IL-1 beta a nd IL-6, was confirmed through use of specific anti-human cytokine IgG antibodies in neutralisation and slot-blot radioimmunoassays. TNF bet a was not detected in the SF by slot-blot radioimmunoassay. These resu lts suggest that a significant increase in intra-articular TNF alpha o ccurs during acute inflammatory arthritis in horses. The lack of corre lation between infiltrating inflammatory cells and SF TNF alpha levels further suggests that the source of TNF alpha may be resident cells o f the joint, as opposed to infiltrating cells found within the joint f luids, SF from clinically normal and arthritic joints of racing and ho spitalised horses were also screened for bioactive TNF alpha. No stati stically significant differences were found in the TNF alpha levels of the normal (29.46 +/- 3.15 u/ml) vs, degenerative (21.64 +/- 3.39 u/m l) joints, although significant elevations were noted in the arthritic joints for SF protein levels and WBC and RBC counts. However, when gr ouped by arthropathy, there were significant differences from normal i n the SF TNF alpha levels in cases of synovitis and major intra-articu lar fractures.