Abstract
In human peripheral blood mononuclear cells, ciliary neurotrophic factor (CNTF) weakly suppressed endotoxin-induced interleukin (IL)-1 and prostaglandin E2(PGE2). Suppression of PGE2 and IL-8 synthesis was significantly greater (up to 42.6%, P < 0.05) by adding a 10-fold molar excess of soluble CNTF receptor (sCNTFR alpha). In cultured human fibroblasts, CNTF at 12 micrograms/ml did not suppress IL-1 alpha-induced IL-8. However, in the presence of a 10-fold excess of sCNTFR alpha, 300 ng/ml of CNTF suppressed IL-1 alpha-induced IL-8 by 44%. Therefore, sCNTFR alpha can confer to CNTF anti-inflammatory properties in vitro. IL-6 which, like CNTF, utilizes the gp130 signal transducer, possesses similar inhibitory effects. That CNTF and IL-6 share gp130 as a receptor component suggests that gp130 mediates these anti-inflammatory responses.
Publication types
-
Research Support, U.S. Gov't, Non-P.H.S.
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Cells, Cultured
-
Ciliary Neurotrophic Factor
-
Cytokines / biosynthesis*
-
Dinoprostone / biosynthesis*
-
Dose-Response Relationship, Drug
-
Fibroblasts / drug effects
-
Fibroblasts / immunology
-
Fibroblasts / metabolism
-
Humans
-
Inflammation
-
Interleukin-1 / biosynthesis*
-
Interleukin-1 / pharmacology
-
Interleukin-8 / biosynthesis
-
Leukocytes, Mononuclear / drug effects
-
Leukocytes, Mononuclear / physiology*
-
Lipopolysaccharides / pharmacology
-
Male
-
Nerve Growth Factors / pharmacology
-
Nerve Tissue Proteins / pharmacology*
-
Receptor, Ciliary Neurotrophic Factor
-
Receptors, Nerve Growth Factor / physiology*
-
Recombinant Proteins / metabolism
-
Recombinant Proteins / pharmacology
-
Skin / drug effects
-
Skin / immunology
-
Skin / metabolism
Substances
-
Ciliary Neurotrophic Factor
-
Cytokines
-
Interleukin-1
-
Interleukin-8
-
Lipopolysaccharides
-
Nerve Growth Factors
-
Nerve Tissue Proteins
-
Receptor, Ciliary Neurotrophic Factor
-
Receptors, Nerve Growth Factor
-
Recombinant Proteins
-
Dinoprostone