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| 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 |
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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.
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Received: 22 August 2016
Published: 25 August 2017
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Corresponding Authors:
WANG Feng
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2017, Vol. 12 
