Toll 样受体 2 通过. 调节肺部炎症和 TNF-α 的释放。

OBJECTIVES: To investigate the roles that Toll-like receptors (TLRs) play in lung inflammation mediated by (MP). METHODS: The changes in TLRs and tumor necrosis factor alpha (TNF-α) in peripheral blood of children with pneumonia (MPP) were monitored, and the interactions of signaling molecules regulating TNF-α release in A549 cells and neutrophils after stimulation were investigated. In TLR2 knockout (TLR2-/-) mice, the levels of TNF-α in bronchial alveolar lavage fluid (BALF) and peripheral blood after mycoplasma infection and the pathological changes in the lung tissue of mice were detected. RESULTS: TNF-α levels in peripheral blood of children with MPP were higher than those in non-infected children, and children with refractory MPP had the highest levels of TNF-α and TLR2. TNF-α secretion and TLR2, myeloid differentiation primary response 88 (MyD88) and phospho-p65(p-p65) levels were increased in stimulated cells. TNF-α secretion was suppressed upon siRNA-mediated TLR2 silencing. Pharmacological inhibition of nuclear factor-kappa B (NF-κB) and MyD88 effectively reduced TNF-α expression. Compared with wild-type mice, the TNF-α in serum and BALF decreased, and lung pro-inflammatory response was partially suppressed in TLR2-/- mice. CONCLUSION: We concluded that TLR2 regulates -mediated lung inflammation and TNF-α release through the TLR2-MyD88-NF-κB signaling pathway.

目的：探讨 Toll 样受体（TLRs）在（MP）介导的肺部炎症中的作用。

方法：监测儿童肺炎支原体肺炎（MPP）患者外周血中 TLRs 和肿瘤坏死因子-α（TNF-α）的变化，研究刺激 A549 细胞和中性粒细胞后调节 TNF-α释放的信号分子之间的相互作用。在 TLR2 基因敲除（TLR2-/-）小鼠中，检测支原体感染后支气管肺泡灌洗液（BALF）和外周血中 TNF-α水平以及小鼠肺组织的病理变化。

结果：MPP 患儿外周血 TNF-α水平高于未感染患儿，难治性 MPP 患儿 TNF-α和 TLR2 水平最高。刺激细胞中 TNF-α分泌和 TLR2、髓样分化初级反应 88（MyD88）和磷酸化 p65（p-p65）水平增加。TLR2 沉默的 siRNA 抑制 TNF-α 分泌。核因子-κB（NF-κB）和 MyD88 的药理学抑制可有效降低 TNF-α表达。与野生型小鼠相比，TLR2-/-小鼠血清和 BALF 中的 TNF-α减少，肺促炎反应部分受到抑制。

结论：我们得出结论，TLR2 通过 TLR2-MyD88-NF-κB 信号通路调节 MP 介导的肺部炎症和 TNF-α释放。