| 刘满菊,王小稳,陈丹,等.Toll样受体 2对儿童肺炎支原体肺炎肺部炎症表现和肿瘤坏死因子 -α的调节作用[J].安徽医药,2024,28(4):680-684. |
| Toll样受体 2对儿童肺炎支原体肺炎肺部炎症表现和肿瘤坏死因子 -α的调节作用 |
| Regulation of TLR2 on pulmonary inflammatory manifestations and TNF-α in children with mycoplasma pneumoniae pneumonia |
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| DOI：10.3969/j.issn.1009-6469.2024.04.009 |
| 中文关键词: 肺炎支原体 Toll样受体 2 肿瘤坏死因子 -α 中性粒细胞 NF-κB |
| 英文关键词: Mycoplasma pneumoniae Toll like receptor 2 (TLR2) Tumor necrosis factor-α (TNF-α) Neutrophils NF-κB |
| 基金项目:河南省医学科技攻关计划项目( LHGJ20190893) |
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| 中文摘要: |
| 目的探讨 Toll样受体 2(TLR2)对肺炎支原体肺炎( MPP)病儿肺部炎症表现和肿瘤坏死因子 -α(TNF-α)的调节作用。方法选取 2021年 1月至 2022年 1月郑州大学附属儿童医院诊治的 MPP病儿 27例，其中难治性肺炎支原体肺炎( RMPP)病儿 12例、 MPP病儿 15例。选取非感染病儿 12例作为对照( NC)组。检测并比较不同病儿外周血 TLR和 TNF-α的表达，培养 A549细胞并比较其与中性粒细胞肺炎支原体( MP)刺激的 TNF-α表达，以及 TLR2敲除后 MP刺激的 TNF-α表达。结果 MPP病儿血清 TNF-α水平高于 NC组，且 RMPP组高于 MPP组( P<0.05)。 RMPP组外周血中性粒细胞 TLR1和 TLR2mRNA高于 MPP组(P<0.05)。 MPP组 TLR2 mRNA高于 NC组( P<0.05)。 MP刺激组的 TNF-α［A549细胞:(19.50±1.30)ng/L，中性粒细胞:(505.60±92.40)ng/L］和 TLR2(A549细胞: 3 760.17±772.06，中性粒细胞: 4 224.00±711.12)表达显著高于 NC组( P<0.05)。 TLR2敲除后 A549细胞后，与对照组相比， TLR2敲除的细胞 MP刺激诱导的 TNF-α表达受到显著抑制。蛋白质印迹法显示， MP刺激 A549细胞中 MyD88和 NF-κB蛋白表达均明显增加( P<0.05)。阻断 Myd88或 NF-κB可明显减弱 MP诱导的 A549细胞 TNF-α表达(P<0.05)。结论 TLR2可调节 MPP通过 TLR2-MyD88-NF-κB信号通路介导的肺部炎症和 TNF-α释放。 |
| 英文摘要: |
| Objective To explore the regulatory effect of Toll like receptor 2 (TLR2) on pulmonary inflammation and tumor necrosis factor-α (TNF-α) in children with mycoplasma pneumoniae pneumonia (MPP).Methods A total of 27 children with MPP who were di? agnosed and treated in Children's Hospital Affiliated to Zhengzhou University from January 2021 to January 2022 were selected, in?cluding 12 children with refractory mycoplasma pneumoniae pneumonia (RMPP) and 15 children with MPP. Twelve cases of non-infect?ed children were selected as control (NC group). The expressions of TLR and TNF-α in peripheral blood of different children were de?tected and compared, and A549 cells were cultured and compared with the expressions of TNF-α stimulated by mycoplasma pneumoni? ae(MP) in neutrophils and after TLR2 knockout.Results The serum level of TNF-α was higher in children with MPP than that in the NC group, and the TNF-α level in the RMPP group was higher than that in the MPP group (P<0.05). The TLR1 and TLR2 mRNAs ofperipheral blood neutrophils in the RMPP group were higher in RMPP group than that in the MPP group (P<0.05). TLR2 mRNA level in MPP group was higher than that in NC group (P<0.05). The expressions of TNF-α [A549 cells: (19.50±1.30) ng/L, neutrophils:(505.60±92.40) ng/L] and TLR2 [A549 cells: (3 760.17±772.06) , neutrophils: (4 224.00±711.12)] in MP stimulation group were signifi?cantly higher than those in NC group (P<0.05). After TLR2 knockout in A549 cells, MP stimulation-induced TNF-α expression inTLR2 knockout cells was significantly inhibited compared with the control group. Western blotting results showed that the protein ex?pressions of MyD88 and NF-κB were significantly increased in A549 cells stimulated by MP (P<0.05). Blocking MyD88 or NF-κB could significantly attenuate MP-induced TNF-α expression in A549 cells (P<0.05).Conclusion TLR2 can regulate the pulmonary in? flammation and TNF-α release mediated by TLR2-MyD88-NF-κB signaling pathway in MPP. |
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