为探讨脓肿分枝杆菌脓肿亚种和马赛亚种经Toll样受体2(Toll-like receptor 2，TLR2)介导的c-Jun氨基末端激酶(c-Jun N-terminal kinase，JNK)和细胞外信号调节激酶(extracellular signal-regulated kinase，ERK)诱导THP-1巨噬细胞内肿瘤坏死因子α(tumor necrosis factor α，TNF-α)和白细胞介素8(interleukin 8，IL-8)表达的相关分子机制，本研究将脓肿分枝杆菌脓肿亚种和马赛亚种感染THP-1巨噬细胞，细菌与巨噬细胞最佳感染之比为感染复数(multiplicity of infection，MOI)＝3，用荧光定量聚合酶链反应(polymerase chain reaction，PCR)检测THP-1巨噬细胞感染两细菌亚种6 h后的胞内TNF-α和IL-8 mRNA水平，以及分别阻断TLR2、JNK 和ERK信号蛋白后TNF-α和IL-8 mRNA水平的变化。结果显示，脓肿分枝杆菌脓肿亚种和马赛亚种作用于THP-1巨噬细胞6 h后，均可诱导细胞内TNF-α和IL-8 mRNA水平显著上调，差异有统计学意义(P＜0.05)；分别阻断TLR2、JNK和ERK信号蛋白，脓肿亚种感染THP-1巨噬细胞后胞内TNF-α和IL-8 mRNA上调水平出现明显抑制，差异有统计学意义(P＜0.05)；分别阻断TLR2和JNK信号蛋白，马赛亚种感染THP-1巨噬细胞后胞内TNF-α和IL-8 mRNA上调水平均出现明显抑制，差异有统计学意义(P＜0.05)；而阻断ERK信号蛋白后，马赛亚种组仅见IL-8 mRNA水平明显抑制，差异有统计学意义(P＜0.05)，而TNF-α mRNA水平未见明显变化，差异无统计学意义(P＞0.05)。本研究提示，脓肿分枝杆菌脓肿亚种和马赛亚种均可作用于TLR2，诱导THP-1细胞内TNF-α和IL-8 mRNA水平上调，脓肿亚种可经JNK和ERK信号蛋白诱导TNF-α mRNA上调，马赛亚种可经JNK信号蛋白诱导TNF-α mRNA上调；脓肿亚种和马赛亚种诱导IL-8 mRNA上调可能与JNK和ERK信号蛋白相关。

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.