Inflammatory Arthritic Diseases Research Articles

Retinoic Acid Effects on Endothelial Cell Function: Interaction with Interleukin 1

Blood vessel angiogenesis is an important component of chronic synovitis, and its regulation may be mediated through local production and effects of certain inflammatory cytokines, including interleukin-1 (IL-1). Retinoic acid (RA) can alter the progression of some inflammatory arthritic diseases, presumably through effects on fibroblast collagenase and PGE 2 production. To explore alternate hypotheses, we examined the interaction of retinoic acid and IL-1 on endothelial cell (EC) function and found that RA directly affects and modifies the effects of IL-1 on EC proliferation, prostacyclin production, and plasminogen activator inhibitor capacity (PAI-1). With respect to EC proliferation, cis- and trans-retinoic acid and retinol induced a dosedependent increase of [ 3H]TdR uptake by cultured ECs, independent of the effects of serum or eicosanoid production. This effect was blocked by IL-1. With respect to EC prostacyclin production, although retinoic acid alone had no effect, cis and trans -retinoic acid and retinol all induced a dose-dependent increase in IL-1-mediated prostacyclin production, which was most marked at higher concentrations (20 U/ml) of IL-1. This effect was mediated through effects independent of cyclooxygenase (COX) production. With respect to plasminogen activator inhibitor capacity, both IL-1 and retinoic acid stimulated EC PAI-1 synthesis, but the individual effects were additive, with RA augmenting the known IL-1 effects on EC PAI-1 production. The interaction between RA and IL-1 on the endothelium, described in this study, may play a role in the fashion through which retinoic acid alters the expression of synovitis in certain types of experimental inflammatory arthritis.

Arthritis and Allied Conditions: A Textbook of Rheumatology.

Introduction to the study of rheumatic diseases scientific basis for the study of the rheumatic diseases clinical pharmacology of anti-rheumatic drugs rheumatoid arthritis other inflammatory arthritic syndromes systematic rheumatic diseases miscellaneous rheumatic diseases regional disorders of joints and related structures osteoarthritis metabolic bone and joint diseases infectious arthritis.

Synovial Cells Responding to a 65‐kDa Mycobacterial Heat Shock Protein have a High Proportion of a TcRγδ Subtype Uncommon in Peripheral Blood

We have analysed the ability of T cells from synovial fluid mononuclear cells (SFMC) and from peripheral blood mononuclear cells (PBMC) of inflammatory arthritic diseases to proliferate in response to mycobacterial antigens (65-kDa heat shock protein [hsp] of BCG, whole BCG) and to rat collagen type II. The SFMC demonstrated a significantly greater ability to respond to 65-kDa hsp of BCG, and to whole BCG, compared with PBMC from the same patients. With collagen type II, only a small proportion of the patients showed a proliferative response, although with this antigen also SFMC responded better than PBMC. There was no difference between SFMC and PBMC in the response to control antigen (tetanus toxoid), phytohaemagglutinin (PHA), or interleukin 2 (IL-2). A high proportion of cells in SFMC-derived short-term T-cell lines were of TcR gamma delta type, often exceeding the number of TcR gamma beta type. There was a significantly higher proportion of TcR gamma delta cells in the SFMC lines compared with the PBMC lines, and a large part of the TcR gamma delta cells in the SFMC cultures was CD8+. The SFMC lines had a high proportion of delta-TCS-1+ cells (V delta 1) among their TcR gamma delta cells, always exceeding the percentages of Ti gamma A+(V gamma 9) and BB3+ (V delta 2). In the PBMC lines, the distribution of TcR gamma delta subtypes was markedly different, with a Ti gamma A+/BB3+ population in the majority. These data argue for a different subpopulation distribution of TcR gamma delta cells in synovial fluid compared with peripheral blood of patients with inflammatory arthritic diseases.

Neutral protease, collagenase and elastase activities in synovial fluids from arthritic patients.

Neutral protease, collagenase and elastase activities were high in synovial fluids from inflammatory arthritic diseases such as gout, active rheumatoid arthritis and ankylosing spondylitis. The activities correlated well with biochemical parameters such as CRP, ESR and total protein. Values were much lower in a non-inflammatory fluid from a patient with osteoarthrosis. Treatment of fluids with trypsin released both collagenase and elastase. The fluids possessed reserve inhibitory action against these enzymes presumably due to plasma antiproteases being present. The collagenase present was found to possess a MW of 32,700 daltons.