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
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.