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Retinoic acid inhibits interleukin‐1‐induced cytokine synthesis in human monocytes
Author(s) -
Gross Volker,
Villiger Peter M.,
Zhang Baoping,
Lotz Martin
Publication year - 1993
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.54.2.125
Subject(s) - retinoic acid , cytokine , biology , monocyte , gene expression , interleukin , lipopolysaccharide , phorbol , endocrinology , signal transduction , microbiology and biotechnology , immunology , biochemistry , protein kinase c , gene
Retinoids are pluripotent morphogens whose effects on gene expression are mediated through specific intracellular receptors. They have certain anti‐inflammatory effects in vivo, the basis of which is not clearly understood. To characterize mechanisms involved with potential anti‐inflammatory actions of retinoids, we studied the effects of retinoic acid (RA) on cytokine production in human peripheral blood monocytes. RA differentially modulated the expression of interleukin‐1β (IL‐10), IL‐6, and IL‐8 mRNAs depending on the inducing stimulus. While phorbol myristate acetate‐induced IL‐lβ and IL‐8 mRNA expression was increased by RA (IL‐6 could not be induced by this pathway in monocytes), IL‐lβ‐induced expression of IL‐1β and IL‐8 was markedly reduced and IL‐6 gene expression was almost completely suppressed. Lipopolysaccharide (LPS)‐induced cytokine synthesis was only slightly reduced and this required a longer preincubation (> 72 h) of monocytes with RA. IL‐l‐induced de novo synthesis of IL‐6 protein and secretion of biologically active IL‐6 were also inhibited by RA. The inhibition pattern of RA was different from that of dexamethasone, which inhibited both IL‐1 and LPS effects. In summary, our data show that RA regulates monocyte cytokine expression selectively in response to the particular stimuli. Inhibition of IL‐lβ‐induced cytokine expression provides a mechanism that can explain some of the anti‐inflammatory effects of RA.