Regulation of haptoglobin expression in a human keratinocyte cell line HaCaT by inflammatory cytokines and dexamethasone.
- Author:
Li-xin XIA
1
;
Ting XIAO
;
Hong-duo CHEN
;
Ping LI
;
Ya-kun WANG
;
He WANG
Author Information
- Publication Type:Journal Article
- MeSH: Cell Line; Dexamethasone; pharmacology; Glucocorticoids; pharmacology; Haptoglobins; analysis; Humans; Interferon-gamma; pharmacology; Interleukin-4; pharmacology; Interleukin-6; pharmacology; Keratinocytes; chemistry; drug effects; Tumor Necrosis Factor-alpha; pharmacology
- From: Chinese Medical Journal 2008;121(8):730-734
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDHaptoglobin (Hp) is one of the acute-phase proteins. Recent studies have demonstrated that Hp exerts immunoregulatory and anti-inflammatory actions and may be one of the inhibitory factors of immune reactions in the skin. In this study we investigated the regulation of Hp expression in a human keratinocyte cell line HaCaT by various cytokines and glucocorticoid.
METHODSHaCaT cells were cultured with IL-6 (50 ng/ml), TNF-alpha (20 ng/ml), IFN-gamma (20 ng/ml) or IL-4 (20 ng/ml) with or without 1 micromol/L dexamethasone in 6-well plates for 12, 24 and 48 hours. Both the cells and the supernatants were collected to detect the changes of Hp expression by reverse-transcription PCR, ELISA and immunohistochemistry.
RESULTSThe results showed that Hp expression were elevated at both the mRNA and protein level by the combination of IL-6, TNF-alpha or IL-4 with dexamethasone, whereas the three cytokines alone did not upregulate the Hp expression. IFN-gamma showed no effect on the Hp expression in HaCaT cells.
CONCLUSIONSThese findings suggest that different inflammatory cytokines as well as glucocorticoid may be involved in the regulation of Hp expression in keratinocytes, and this may be one of the negative feedback mechanisms in inflammatory skin diseases.