Theanine improves the function of dendritic cells via the downregulation of cyclooxygenase-2 expression.
- Author:
Mingsheng LEI
1
,
2
;
Jianhong ZUO
3
;
Min LI
4
;
Qihua GU
4
;
Chengping HU
5
Author Information
- Publication Type:Journal Article
- MeSH: Bombesin; pharmacology; Cells, Cultured; Cyclooxygenase 2; metabolism; Dendritic Cells; drug effects; metabolism; Enzyme-Linked Immunosorbent Assay; Glutamates; pharmacology; Humans; Interleukin-10; metabolism; Interleukin-12; metabolism
- From: Chinese Medical Journal 2014;127(8):1545-1549
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDTumor cells can reduce the number of dendritic cells (DCs) in the tumor environment and cause DC dysfunction through autocrine or paracrine pathways. We sought to measure cyclooxygenase-2 (COX-2) expression in bombesin-inhibited DCs treated with theanine in vitro and to explore the protection and activation effects of theanine on DCs.
METHODSEnzyme-linked immunosorbent assay (ELISA), reverse transcription-polymerase chain reaction (RT-PCR), and Western blotting were used to analyze the effects of theanine on COX-2 expression and interleukin (IL)-12/IL-10 secretion of bombesin-treated DCs.
RESULTSDCs acquired an impaired phenotype as a result of bombesin treatment. Theanine increased the expression of mature DC surface molecules. The number of cell apoptosis with the treatment of bombesin and theanine significantly decreased, accounting for 15.9%, compared with 26.1% of cell apoptosis with bombesin. COX-2 expression in bombesin-treated DCs was inhibited by theanine in a dose-dependent manner. Theanine promoted DC secretion of IL-12. IL-12 levels reached (137.4 ± 4.9) pg/ml with theanine at 200 µmol/L. However, theanine inhibited the secretion of IL-10 in a dose-dependent manner. IL-10 levels were only (58.4 ± 6.9) pg/ml with theanine at 200 µmol/L.
CONCLUSIONTheanine inhibits the transcription and translation of COX-2 and regulates the balance of IL-10/IL-12 secretion in bombesin-inhibited DCs, leading to the recovery of a state of activation in DCs.