THE ROLES AND RELATED MECHANISMS FOR EXPLORING CHLAMYDIA TRACHOMATIS CT849 PROTEIN IN THE PROCESS OF REGULATION OF HOST CELL INFLAMMATION

Wen Cen, Yan Ma

Department of Dermatology & STD, Second Hospital of Shanxi Medical University, Taiyuan, PR China

Purpose: This paper analysed the role and related mechanisms of chlamydia trachomatis CT849 protein in the regulation of host cell inflammation. 

Method: THP-1 cells were pre-treated with PMA (100 ng/ml) and differentiated into adherent macrophages, CT849 protein stimulating adherent cells. The changes of TNF-α, IL-1β, IL-6 and IL-8 in the THP-1 cells supernatant were detected by ELISA. THP-1 cells were pre-treated with ERK inhibitors and JNK inhibitors for 24 hours, then stimulated with CT849 protein (10 g/ml) for 24 hours, and then the phosphorylation levels of ERK and JNK were detected by Western blotting. THP-1 cells were pre-treated with ERK and JNK blockers. The levels of cytokines (NF-α, IL-1βa, IL-6 and IL-8) were detected by ELISA. 

Result: The contents of TNF-α, IL-1βa, IL-6 and IL-8 increased in a dose-dependent manner after TNP-1 cells were induced by different concentrations of CT849 protein. Treated with 10 μg/ml CT849, the expression level of TNF-α reached the peak after 12 h stimulation, and the expression levels of IL-1β, IL-6 and IL-8 reached the peak after 24 h stimulation. The results of Western blotting showed that the phosphorylation levels of ERK and JNK in CT849 protein treatment group were significantly higher than those in the control group. The results of ERK and JNK blockers on THP-1 cells showed that ERK and JNK blockers could significantly inhibit CT849 protein from producing TNF-α, IL-1βa, IL-6 and IL-8, compared with those treated by CT849 protein. There were significant statistical differences (P<0.05). 

Conclusion: Chlamydia trachomatis CT849 protein can significantly promote the secretion of inflammatory factors (TNF-α, IL-1βa, IL-6 and IL-8) produced by host cells, and the related mechanism may be related to the activation of ERK and JNK signal transduction pathways.