Stimulated expressions of tumor necrosis factor α and interleukin 8 in macrophages challenged by Mycobacterium abscessus through TLR2, JNK and ERK pathways
GUI Jing, WANG Feng, LI Qing, LI Jinli
Department of Pathogenic Laboratory, Shenzhen Center for Chronic Disease Control, Shenzhen 518020, China
Abstract：The purpose of the current study is to investigate the molecular mechanisms of tumor necrosis factor α (TNF-α) and interleukin 8 (IL-8) mRNA expressions in THP-1 macrophages challenged by Mycobacterium abscessus subsp. abscessus (Mabs) and Mycobacterium abscessus subsp. massiliense (Mmass). The role of Toll-like receptor 2 (TLR2)-mediated c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) signaling pathways were investigated. First, THP-1 macrophages were cultured in the presence of Mabs and Mmass to stimulate cytokine expression . The mRNA expression levels of TNF-α and IL-8 were analyzed using quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) after 6 h. The levels of TNF-α and IL-8 mRNA after administration of anti-TLR2 mAb, JNK signaling inhibitor SP600125 and ERK signaling inhibitor U0126 were also detected. The results demonstrated that the levels of TNF-α and IL-8 mRNA in THP-1 cells were significantly upregulated by Mabs and Mmass for 6 h (P<0.05). The stimulated expressions of both TNF-α and IL-8 were significantly downregulated by anti-TLR2 mAb, JNK inhibitor or ERK inhibitor, respectively. It was thus concluded that both Mabs and Mmass could upregulate TNF-α and IL-8 mRNA expressions through TLR2-mediated JNK and ERK pathways.
桂静，王峰，李青，李金莉. 脓肿分枝杆菌经Toll样受体2介导的JNK/ERK信号通路诱导巨噬细胞表达肿瘤坏死因子α和白细胞介素8[J]. 微生物与感染, 2017, 12(4): 211-216.
GUI Jing, WANG Feng, LI Qing, LI Jinli. Stimulated expressions of tumor necrosis factor α and interleukin 8 in macrophages challenged by Mycobacterium abscessus through TLR2, JNK and ERK pathways. JOURNAL OF MICROBES AND INFECTIONS, 2017, 12(4): 211-216.
2017, Vol. 12 
