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  • Title: In vitro effects of erythromycin on RANKL and nuclear factor-kappa B by human TNF-alpha stimulated Jurkat cells.
    Author: Wu L, Lin JH, Bao K, Li PF, Zhang WG.
    Journal: Int Immunopharmacol; 2009 Aug; 9(9):1105-9. PubMed ID: 19500694.
    Abstract:
    The receptor activator of NF-kappaB ligand (RANKL) and its signal downstream nuclear factor-kappaB (NF-kappaB) are critical regulators for immune responses as well as bone remodeling. The present study aimed to examine the effects of erythromycin (EM) on the activation of RANKL, correlation with NF-kappaB expression, proliferation and apoptosis of human Jurkat T cells. Jurkat T cells were pretreated with 100 pmol/l tumor necrosis factor-alpha (TNF-alpha) for 1 h followed by various concentrations of EM for 24 h. The mRNA expressions of RANKL and NF-kappaB were examined by RT-PCR. The protein expression of NF-kappaB was analyzed by Western blot. The protein level of RANKL was examined by flow cytometry, immunofluorescence microscopy and Western blot analyses. We also examined proliferation of Jurkat T cells by MTT assay, apoptosis by flow cytometry analysis after staining with PI and morphological observation after AO/EB staining. The results showed that EM inhibited TNF-alpha-induced expressions of RANKL and NF-kappaB at both mRNA and protein levels in a concentration-dependent manner. The expression of RANKL was correlated with the expression of NF-kappaB. Moreover, EM influenced the proliferation and apoptosis of human Jurkat T cells. These data suggest that EM acts as an anti-inflammatory agent not only to interact with the expression of NF-kappaB and the proliferation of human Jurkat T cells, but also to reduce the level of RANKL.
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