Experiments have demonstrated the regulation of long noncoding RNA (lncRNA) in tuberculosis (TB), and negative pressure treatment has been associated with the alleviation of TB. Here, we investigated the interaction of negative pressure and the lncRNA X-inactive specific transcript (XIST) in modulating Mycobacterium tuberculosis (MTB) infection. Initially, we established an in vitro cell model of MTB infection and an in vivo mouse model of MTB infection, followed by treatment with negative pressure. Then, we examined the expression of XIST, followed by analysis of the downstream miRNA of XIST. XIST was overexpressed or underexpressed through cell transfection to examine its effects on macrophage polarization via the miR–125b–5p/A2 axis. The MTB models were characterized by upregulated XIST and downregulated miR-125b-5p. XIST bound to miR-125b-5p, leading to its downregulation, and thus causing higher MTB survival in an ESAT-6–dependent manner. Additionally, negative pressure treatment decreased MTB-driven XIST expression through downregulation of A20 (an NF-κB repressor) via miR-125b-5 expression, promoting the M1 polarization program in macrophages through activation of the NF-κB pathway. In summary, negative pressure treatment after MTB infection can promote the polarization of macrophages to the proinflammatory M1 phenotype by regulating the XIST/miR–125b–5p/A20/NF–κB axis.

中文翻译：

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负压通过 lncRNA XIST/microRNA-125b-5p/A20/NF-κB 轴促进结核分枝杆菌感染后巨噬细胞 M1 极化

实验证明了长链非编码 RNA (lncRNA) 在结核病 (TB) 中的调节作用，负压治疗与结核病的缓解有关。在这里，我们研究了负压和 lncRNA X 非活性特异性转录物 (XIST) 在调节结核分枝杆菌(MTB) 感染中的相互作用。最初，我们建立了MTB 感染的体外细胞模型和体内MTB 感染小鼠模型，然后进行负压治疗。然后，我们检查了 XIST 的表达，然后分析了 XIST 的下游 miRNA。XIST 通过细胞转染过表达或过表达，以通过 miR-125b-5p/A2 轴检查其对巨噬细胞极化的影响。MTB 模型的特点是上调 XIST 和下调 miR-125b-5p。XIST 与 miR-125b-5p 结合，导致其下调，从而以 ESAT-6 依赖性方式导致更高的 MTB 存活率。此外，负压治疗通过 miR-125b-5 表达下调 A20（一种 NF-κB 阻遏物）来降低 MTB 驱动的 XIST 表达，通过激活 NF-κB 通路促进巨噬细胞中的 M1 极化程序。总之，