[Erythromycin inhibits elastin peptides-induced differentiation of CD4⁺T cells into Th17 cells]

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2015 Mar;31(3):289-92.
[Article in Chinese]

Abstract

Objective: To investigate the effect of erythromycin on differentiation into T helper 17 (Th17) cells from CD4⁺T cells exposed to elastin peptides.

Methods: The CD4⁺T cells from spleen of male BALB/c mice by magnetic bead sorting were randomly divided into the control group (group A), the elastin peptides group (group B) and erythromycin group(group C). The cells in group B and C were cultured in serum-free medium supplemented with 30 μg/mL elastin peptides. The cells in group C were additionally administrated with erythromycin at a dose of 100 μg/mL. All of the CD4⁺T cells were cultured in serum-free culture solution for 24 hours. The number of the Th17 cells was detected by flow cytometry and the expression of retinoic acid related orphan nuclear receptor γt (RORγt) mRNA was measured by fluorescence quantitative PCR in each group. The expressions of NF-κB(p65) and signal transducer and activator of transcription 3 (STAT3) were analyzed by Western blotting.

Results: The Th17 cells in group B [(11.32 ± 2.34)%] increased as compared with that in group A [(5.21 ± 1.36)%], and the expression of RORγt mRNA in group B was higher than that in group A. Furthermore, the expressions of NF-κB(p65) and STAT3 proteins in group B increased significantly as compared with those in group A. However, compared with group B, group C presented with the significantly decreased expressions of Th17 cells, RORγt mRNA, NF-κB(p65) and STAT3 proteins.

Conclusion: Erythromycin can suppress the differentiation into Th17 cells from CD4⁺T cells exposed to elastin peptides.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CD4-Positive T-Lymphocytes / cytology*
  • CD4-Positive T-Lymphocytes / metabolism
  • Cell Differentiation / drug effects*
  • Cells, Cultured
  • Elastin / metabolism*
  • Erythromycin / pharmacology*
  • Male
  • Mice
  • Mice, Inbred BALB C
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • STAT3 Transcription Factor / genetics
  • STAT3 Transcription Factor / metabolism
  • Th17 Cells / cytology*
  • Th17 Cells / metabolism

Substances

  • NF-kappa B
  • STAT3 Transcription Factor
  • Erythromycin
  • Elastin