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Effects of Cyclic GMP‐Agonists on Ciclosporin‐Induced Suppression of Human Lymphokine Production
Author(s) -
Svenson M.,
Bendtzen K.
Publication year - 1985
Publication title -
allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.363
H-Index - 173
eISSN - 1398-9995
pISSN - 0105-4538
DOI - 10.1111/j.1398-9995.1985.tb00262.x
Subject(s) - lymphokine , medicine , sodium azide , endocrinology , chemistry , cyclic gmp , interleukin 2 , peripheral blood mononuclear cell , agonist , cytokine , pharmacology , biochemistry , biology , in vitro , receptor , enzyme
Ciclosporin (Cs) inhibits the elaboration of the lymphokine leukocyte migration inhibitory factor (LIF) from human blood mononuclear cells (MNC) stimulated with recall antigen. This inhibition was counteracted by 3 × lO ‐5 M dibutyryl‐cyclic GMP and 8‐bromo‐eyclic GMP and by the cyclic GMP‐agonists, sodium nitroprausside (NaNPr), ascorbic acid (As A), sodium azide (NaN 3 ) and carbacholine. Using 5 × 10 ‐5 M NaNPr, 1 × 10 ‐3 M NaN 3 , or 3 × 10 ‐3 M As A, 25–50‐, 4–8‐ and 2–3‐fold elevations of MNC and T‐lymphocyte cyclic GMP‐levels were obtained independently of the presence of Cs. NaNPr was the most potent of these three cyclic GMP‐agonists in counteracting the effect of Cs. The results indicate that intracellular cyclic GMP is a major factor involved in the reversal of Cs induced inhibition of LIF‐production. None of the cyclic GMP‐analogues or ‐agonists by themselves possessed Interleukin 1‐like activity, measured by their ability to induce LIF‐production by macrophage‐depleted T‐lymphocytes challenged by recall antigen.