Prolactin increases tumor necrosis factor alpha expression in peripheral CD14 monocytes of patients with rheumatoid arthritis

• Published in: Cellular immunology 2014-07, Vol.290 (1), p.164-168
• Main Authors: Tang, Chun, Li, Yun, Lin, Xiaojun, Ye, Jinghua, Li, Weinian, He, Zhixiang, Li, Fangfei, Cai, Xiaoyan
• Format: Article
• Language: English
• Subjects: Arthritis, Rheumatoid - immunology; Flavonoids - pharmacology; Gene Expression Regulation - immunology; Gene Silencing; Humans; Lipopolysaccharide Receptors - biosynthesis; MAP Kinase Signaling System - immunology; Methylation specific PCR; Mitogen activated protein; Monocytes - immunology; p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors; p38 Mitogen-Activated Protein Kinases - immunology; Prolactin; Prolactin - metabolism; Protein Kinase Inhibitors - pharmacology; Receptors, Prolactin - genetics; Receptors, Prolactin - immunology; Rheumatoid arthritis; Tumor Necrosis Factor-alpha - biosynthesis; Tumor Necrosis Factor-alpha - immunology; Tumor necrosis factor-α
• ISSN: 0008-8749; 1090-2163
• DOI: 10.1016/j.cellimm.2014.06.005

•CD14+ cells express prolactin receptor.•Prolactin receptors are increased in rheumatoid arthritis patients.•Activating the prolactin receptor induces release of TNF-α from CD14+ cells. Tumor necrosis factor (TNF)-α is one of the major proinflammatory mediators of rheumatic arthritis (RA); the regulatory factors for TNF-α release is not fully understood. This study aims to investigate the role of prolactin receptor (PRLR) activation in regulating the expression and release of TNF-α from CD14+ monocytes. The results showed that the expression of PRLR was detectable in CD14+ monocytes of healthy subjects, which was markedly increased in RA patients. Exposure to PRL in the culture increased the expression and release of TNF-α from CD14+ monocytes, which was abolished by the PRLR gene silencing or blocking the mitogen activated protein (MAPK) pathway. We conclude that exposure to PRL increases TNF-α release from CD14+ monocytes of RA patients, which can be abolished by PRLR gene silencing or treating with MAPK inhibitor.