Premium
THALIDOMIDE ENHANCES SUPEROXIDE ANION RELEASE FROM HUMAN POLYMORPHONUCLEAR AND MONONUCLEAR LEUKOCYTES
Author(s) -
Nielsen H.,
Valerius N. H.
Publication year - 1986
Publication title -
acta pathologica microbiologica scandinavica series c: immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0108-0202
DOI - 10.1111/j.1699-0463.1986.tb02117.x
Subject(s) - superoxide , thalidomide , respiratory burst , chemotaxis , incubation , peripheral blood mononuclear cell , stimulation , mononuclear phagocyte system , immunology , chemistry , monocyte , chronic granulomatous disease , phagocyte , in vitro , biochemistry , pharmacology , medicine , endocrinology , immune system , receptor , multiple myeloma , enzyme
The effect of thalidomide on the function of human polymorphonuclear leukocytes (PMNs) and blood monocytes was tested in vitro. The chemotactic and spontaneous migration was not affected by thalidomide between 0.001 and 0.1 mg/ml. PMN oxygen consumption was not changed after pre‐incubation with thalidomide. However, superoxide anion release upon stimulation of the cells with phorbol‐myristate‐acetate or the chemotactic tripeptide N‐f‐Methionyl‐Leucyl‐Phenylalanine was enhanced in a dosedependent manner after pre‐incubation with thalidomide. Both PMNs and monocytes were influenced. Leukocytes from two patients with chronic granulomatous disease (defective in oxidative burst response) remained unable to produce superoxide anion after pre‐incubation with thalidomide. Thus, we suggest that thalidomide primes the phagocytes to respond with an enhanced superoxide anion release upon stimulation. These findings do not explain the anti‐inflammatory effect of thalidomide but could have relevance in conditions with quantitative defects in phagocyte oxidative responsiveness.