IL-17 Promotes Nitric Oxide Production in Non-Small-Cell Lung Cancer.

IL-17 Promotes Nitric Oxide Production in Non-Small-Cell Lung Cancer.
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DOI:
10.3390/jcm10194572
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发表时间:
2021-10-01
影响因子:
3.9
通讯作者:
Brussino L
Brussino L
中科院分区:
医学2区
文献类型:
--
作者:
Nicola S;Ridolfi I;Rolla G;Filosso P;Giobbe R;Boita M;Culla B;Bucca C;Solidoro P;Brussino L

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肺癌是世界上第二常见的恶性肿瘤,但其病因尚不清楚。炎性细胞因子和Th细胞,包括Th17,现在被发现参与非小细胞肺癌通路,因此假设IL-17通过刺激血管内皮生长因子和一氧化氮的释放在肿瘤血管生成中起作用。尽管许多生物标志物被用于胸部恶性肿瘤的诊断,但关于非小细胞肺癌中FeNO水平和炎症细胞因子的数据仍然很少。我们的研究旨在评估早期NSCLC患者EBC中肺一氧化氮生成与VEGF和th17相关细胞因子的关系。方法:对NCSLC患者和对照组进行FeNO测定和肺功能检查;同时取EBC样本,检测Th1 (IL-1、IL-6、IL-12、IFN-g、TNF-a)、Th17 (IL-17、IL-23)和Th2 (IL-4、IL-5、IL-13)相关细胞因子。结果:除ifn - γ和tnf - α外,患者EBC中Th1和th17相关细胞因子显著高于健康对照组,而th2相关细胞因子未见差异。非小细胞肺癌患者中FeNO、JawNO和CalvNO水平在50 mL/s流速下明显高于对照组。FeNO 50 mL/s与IL-17、IL-1、VEGF呈显著相关。JawNO水平与IL-6、IL-17、VEGF呈正相关。FeNO与th2相关细胞因子之间无相关性。结论:这是第一份评估早期NSCLC患者EBC中FeNO水平与th17相关细胞因子之间关系的报告。IL-17通过VEGF途径促进血管生成,可能是NSCLC患者肺NO生成增加的间接原因。
Introduction: Lung cancer is the second most frequent malignancy worldwide, but its aetiology is still unclear. Inflammatory cytokines and Th cells, including Th17, are now emerging as being involved in NSCLC pathways, thus postulating a role of IL-17 in tumour angiogenesis by stimulating the vascular endothelial growth factor and the release of nitric oxide. Despite the fact that many biomarkers are used for chest malignancy diagnosis, data on FeNO levels and inflammatory cytokines in NSCLC are still few. Our study aimed to evaluate the relationship between pulmonary nitric oxide production and VEGF and Th17-related cytokines in the EBC of patients affected by early-stage NSCLC. Methods: FeNO measurement and lung function tests were performed in both patients affected by NCSLC and controls; EBC samples were also taken, and Th1 (IL-1, IL-6, IL-12, IFN-g, TNF-a), Th17 (IL-17, IL-23) and Th2 (IL-4, IL-5, IL-13) related cytokines were measured. Results: Th1 and Th17-related cytokines in EBC, except for IFN-gamma and TNF-alpha, were significantly higher in patients than in healthy controls, whereas no differences were seen for Th2-related cytokines. FeNO at the flow rate of 50 mL/s, JawNO and CalvNO levels were significantly higher in patients affected by NSCLC compared to controls. Significant correlations were found between FeNO 50 mL/s and IL-17, IL-1 and VEGF. JawNO levels positively correlated with IL-6, IL-17 and VEGF. No correlations were found between FeNO and Th2-related cytokines. Conclusion: This is the first report assessing a relationship between FeNO levels and Th17-related cytokines in the EBC of patients affected by early-stage NSCLC. IL-17, which could promote angiogenesis through the VEGF pathway, might be indirectly responsible for the increased lung production of NO in patients with NSCLC.
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