dinoprost and Autoimmune-Diseases

To evaluate the occurrence and clinical significance of lipid peroxidation (oxidative stress) in rheumatic diseases characterized by vascular involvement.. Plasma 8-epi-PGF2alpha (oxidative stress marker) was measured by gas chromatography-mass spectrometry in 36 patients with systemic lupus erythematosus (SLE), 13 with systemic sclerosis (SSc), 13 with systemic vasculitis [Wegener's granulomatosis (WG), n = 4; Churg Strauss syndrome (CSS), n = 3; Behcet syndrome, n = 6], 12 with rheumatoid arthritis (RA) and in 23 healthy controls (n = 23).. 8-epi-PGF2alpha levels were higher in patients with SLE (P = 0.007), SSc (P < 0.001) and vasculitis (P = 0.001) than in controls. In SLE, a positive Coombs' test and arterial hypertension independently predicted 8-epi-PGF2alpha concentrations (P = 0.004 and P = 0.001, respectively). SLE patients not taking prednisolone showed higher 8-epi-PGF2alpha concentrations than SLE patients on prednisolone (P = 0.02). In the latter group, a dose response relationship was noted between 8-epi-PGF2alpha and steroid dosage (r = 0.6, P = 0.0003). In WG and CSS, 8-epi-PGF2alpha concentrations correlated with disease activity (r = 0.8, P = 0.01) and were higher than in patients with Behcet disease (P = 0.003).. Oxidative stress may be pathogenetically relevant in some autoimmune rheumatic diseases with vascular involvement. Amelioration of some clinical manifestations of these diseases may be envisaged by targeting lipid peroxidation with dietary or pharmacological antioxidants.

Topics: Adult; Aged; Autoimmune Diseases; Dinoprost; Female; Humans; Lipid Peroxidation; Lupus Erythematosus, Systemic; Male; Middle Aged; Oxidative Stress; Vascular Diseases; Vasoconstrictor Agents

The important role played by prostaglandins in the pathogenesis of coronary disease and essential hypertension is well known. The authors have attempted to reveal a relationship between blood levels of natural autoantibodies to PGF2 alpha and PGE2 and specific features of coronary disease and essential hypertension course and complications. A total of 87 subjects were examined, 23 of these--normal controls, 25 patients with myocardial infarction, 22 with angina pectoris, and 17 with essential hypertension. Solid-phase enzyme immunoassay was employed to detect anti-PGF2 alpha and anti-PGE2 antibodies. These antibodies were found in normal subjects, coronary patients and hypertensives. Blood levels of these antibodies correlated with some complications of coronary disease and essential hypertension. These results permit a hypothesis that the pathogenetic physiologic role of the detected natural antibodies to prostaglandins consists in their defense homeostatic function.

Topics: Adult; Aged; Autoantibodies; Autoimmune Diseases; Coronary Disease; Dinoprost; Dinoprostone; Humans; Hypertension; Middle Aged

Immunosuppressive effects of E-series prostaglandins have been demonstrated in many in vitro assays of immune responsiveness as well as in autoimmune diseases. To explore the mechanisms underlying prostaglandin E1 (PGE1)-associated immunosuppression in autoimmunity, we treated SJL mice immunized to produce immune-mediated interstitial nephritis with PGE1, PGF2 alpha, or vehicle alone. Mice receiving PGE1 treatment do not develop interstitial nephritis, nor do they display delayed-type hypersensitivity (DTH) to the immunizing renal tubular antigen preparation. The observed immunosuppression is critically dependent on PGE1 administration during the period of effector T cell induction. We therefore investigated the effect of PGE1 on the in vitro induction of DTH effector T cells reactive to renal tubular antigens (SRTA). PGE1 inhibits effector T cell induction in a dose-dependent, reversible manner, but has no inhibitory effect on fully differentiated DTH effector cells or SRTA-reactive cell lines. The PGE1 effect is indirect and mediated via nonspecific suppressor lymphokines. This suppression can be overcome by recombinant interleukin 1 (IL-1), which suggests a mechanism related to either diminished IL-1 secretion or target cell sensitivity to IL-1.

Topics: Alprostadil; Animals; Antigens; Autoimmune Diseases; Basement Membrane; Dinoprost; Hypersensitivity, Delayed; Immunization; Interleukin-1; Kidney Tubules; Mice; Nephritis, Interstitial; Prostaglandins F; Rabbits; Recombinant Proteins; T-Lymphocytes; T-Lymphocytes, Helper-Inducer

The New Zealand Black (NZB) mouse is a model animal for human autoimmune disease. Abnormalities in Interleukin 2 (IL-2) production were studied in these mice to investigate whether they arise from disorders in T cells or from abnormalities of macrophages (M phi). T cells were separated from thymocytes using peanut agglutinin (PNA), while M phi were separated from spleen cells using the adherence method. Cultures were prepared from T cells and M phi obtained from normal control mice and NZB mice and the activity of IL-2 in the supernatant of the culture was studied. The results indicate that abnormalities in the production of IL-2 in NZB mice are due to functional disorders in both T cells and M phi.

Topics: Animals; Autoimmune Diseases; Cells, Cultured; Dinoprost; Dinoprostone; Indomethacin; Interleukin-1; Interleukin-2; Lectins; Macrophages; Male; Mice; Mice, Inbred BALB C; Mice, Inbred CBA; Mice, Inbred NZB; Peanut Agglutinin; Prostaglandins E; Prostaglandins F; T-Lymphocytes