CELL TRAFFICKING, MEDIATOR RELEASE, AND ARTICULAR METABOLISM IN ACUTE-INFLAMMATION OF INNERVATED OR DENERVATED ISOLATED EQUINE JOINTS

Citation
J. Hardy et al., CELL TRAFFICKING, MEDIATOR RELEASE, AND ARTICULAR METABOLISM IN ACUTE-INFLAMMATION OF INNERVATED OR DENERVATED ISOLATED EQUINE JOINTS, American journal of veterinary research, 59(1), 1998, pp. 88-100
Citations number
41
Categorie Soggetti
Veterinary Sciences
ISSN journal
00029645
Volume
59
Issue
1
Year of publication
1998
Pages
88 - 100
Database
ISI
SICI code
0002-9645(1998)59:1<88:CTMRAA>2.0.ZU;2-T
Abstract
Objectives-To describe the acute cellular response, inflammatory media tor release, and effect on chondrocyte metabolism of interleukin 1 bet a (IL-1 beta) in isolated innervated or denervated equine metacarpopha langeal joints. Animals-One metacarpophalangeal joint of 24 adult hors es. Procedures-The metacarpophalangeal joint was isolated for 6 hours in a pump-perfused, auto-oxygenated, innervated or denervated metacarp ophalangeal joint preparation. Isolated joints were assigned to 4 grou ps: control, control-denervated, inflamed, and inflamed-denervated, an d inflammation was induced by intra-articular injection of IL-1 beta. Synovial fluid was collected for cytologic examination and determinati on of IL (IL)-1 beta, (IL-6), prostaglandin E-2 (PGE(2)), and substanc e P (SP) values. Synovial membrane was immunostained with SP and nerve -specific enolase (NSE) antibodies. Cartilage was collected for determ ination of proteoglycan (PG) synthesis and degradation. Results-IL-1 b eta induced significant neutrophilic leukocytosis in synovial fluid an d synovial membrane. IL-1 beta concentration had returned to baseline by 5.5 hours, but IL-6 concentration significantly increased throughou t the study. Total SP content was significantly higher in inflamed joi nts. There was a significant increase in 24- and 48-hour PG degradatio n in inflamed innervated joints. Conclusion-Cellular response to IL-1 beta was rapid and sustained; joint clearance of IL-1 beta was rapid, and endogenous production of IL-1 beta did not follow. The IL-6 and PG E(2) concentrations significantly increased, and SP content was increa sed in association with inflammation but not denervation. A degradativ e response of cartilage to IL-1 beta was observed, and was enhanced by innervation. This model was useful for investigation of the articular response to acute inflammation and the influence of denervation in mo dulating this response.