Abstract
Human keratinocytes (HK) generate nitric oxide (NO) and proinflammatory mediators following activation with either IgE/anti-IgE immune complexes or a combination of lipopolysaccharide (LPS) and interferon-gamma (IFN-gamma). Recently, interleukin-10 (IL-10) has been shown to down-regulate various inflammatory responses and to be secreted by lymphocytes and dendritic cells during skin inflammatory reactions. We show here that IL-10 down-regulates the production of tumor necrosis factor (TNF)-alpha and IL-6 by activated HK. Also, induction of inducible nitric oxide synthase (iNOS) expression in HK by IgE/anti-IgE or LPS/IFN-gamma is significantly reduced by the addition of IL-10. This effect is dose dependent and correlates with reduction of iNOS mRNA production and enzyme level. Therefore, IL-10 down-regulates NO-mediated HK inflammatory responses and may thus participate in the regulation of the skin immune network.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Antibodies, Anti-Idiotypic / pharmacology
-
Base Sequence
-
Cells, Cultured
-
Depression, Chemical
-
Enzyme Induction / drug effects
-
Gene Expression Regulation / drug effects*
-
Humans
-
Immunoglobulin E / pharmacology*
-
Interferon-gamma / pharmacology
-
Interleukin-10 / pharmacology*
-
Interleukin-6 / biosynthesis*
-
Interleukin-6 / genetics
-
Interleukin-6 / metabolism
-
Keratinocytes / drug effects*
-
Keratinocytes / enzymology
-
Lipopolysaccharides / pharmacology
-
Molecular Sequence Data
-
Nitric Oxide / biosynthesis
-
Nitric Oxide Synthase / biosynthesis*
-
Recombinant Proteins
-
Tumor Necrosis Factor-alpha / biosynthesis*
-
Tumor Necrosis Factor-alpha / genetics
-
Tumor Necrosis Factor-alpha / metabolism
Substances
-
Antibodies, Anti-Idiotypic
-
Interleukin-6
-
Lipopolysaccharides
-
Recombinant Proteins
-
Tumor Necrosis Factor-alpha
-
anti-IgE antibodies
-
Interleukin-10
-
Nitric Oxide
-
Immunoglobulin E
-
Interferon-gamma
-
Nitric Oxide Synthase