CCL-18、IL-8 在 COPD 并发肺动脉高压的相关性研究

张(包头医学院第一附属医院，中国)
垚(包头医学院第一附属医院，中国)
连生 党(包头医学院第一附属医院，中国)

摘要

肺动脉高压（PH）是慢性阻塞性肺疾病（COPD）终末期严重并发症，其机制涉及低氧、炎症及肺血管重塑等。趋化因子CCL-18和IL-8通过调控炎症细胞募集与激活，在COPD-PH中发挥关键性作用。CCL-18可诱导巨噬细胞向M2型极化，使其分泌炎性因子促进平滑肌增殖。此外，CCL-18还能通过特定信号通路增强成纤维细胞的增殖活性，共同加剧肺血管重塑过CCL-18的上述作用。IL-8通过激活其特异性受体，触发下游信号通路，促进中性粒细胞浸润、血管内皮损伤及平滑肌细胞增殖，从而加剧肺动脉高压的进展。在细菌感染情况下，IL-8可进一步放大炎症反应，加重病理进程。CCL-18与IL-8的相互协同放大炎症级联反应，其联合检测有望成为COPD-PH的预测标志物和治疗靶点。

关键词

慢性阻塞性肺疾病；肺动脉高压；肺部活化激活调节趋化因子；白细胞介素-8

参考

慢性阻塞性肺疾病（COPD）诊治规范（草案） : [J]. 中华结核和呼吸杂志,1997,20(04)：199-203.

Adeloye D, Song P, Zhu Y, et al. Global, regional, and national prevalence of, and risk factors for, chronic obstructive pulmonary disease (COPD) in 2019: a systematic review and modelling analysis. Lancet Respir Med.2022;10(5):447-458.

张嘉莹,樊勇,张卓莉.肺动脉高压发病机制中的肺血管重塑[J]. 中华临床免疫和变态反应杂志,2023,17(01):50-55.

Brock M, Trenkmann M, Gay RE, et al. Interleukin-6 modulates the expression of the bone morphogenic protein receptor type II through a novel STAT3-microRNA cluster 17/92 pathway. Circ Res. 2009;104(10):1184-1191.

杨凌婧 . 稳定期中重度慢阻肺患者血清 IL-6 、 IL-8 、TNF-α、hs-CRP与肺功能的相关性研究[J].临床肺科杂志,2016,21(03):481-484.

高远生 . 一氧化氮信号通路与血管功能 [J]. 生理科学进展,2017,48(01):58-62.

Sheikh AQ, Lighthouse JK, Greif DM. Recapitulation of developing artery muscularization in pulmonary hypertension. Cell Rep. 2014;6(5):809-817.

Muñoz-Esquerre M, Aliagas E, López-Sánchez M, et al. Vascular disease in COPD: Systemic and pulmonary expression of PARC (Pulmonary and Activation-Regulated Chemokine). PLoS One. 2017;12(5):e0177218.

Atamas SP, Luzina IG, Choi J, et al. Pulmonary and activation regulated chemokine stimulates collagen production in lung fibroblasts. Am J Respir Cell Mol Biol. 2003;29(6):743-749.

Catusse J, Wollner S, Leick M, Schröttner P, Schraufstätter I, Burger M. Attenuation of CXCR4 responses by CCL18 in acute lymphocytic leukemia B cells. J Cell Physiol. 2010;225(3):792-800.

Bu T, Wang LF, Yin YQ. How Do Innate Immune Cells Contribute to Airway Remodeling in COPD Progression? Int J Chron Obstruct Pulmon Dis. 2020 Jan 10;15:107-116.

Al-Alwan LA, Chang Y, Mogas A, et al. Differential roles of CXCL2 and CXCL3 and their receptors in regulating normal and asthmatic airway smooth muscle cell migration. J Immunol. 2013;191(5):2731-2741.

Korbecki J, Olbromski M, Dzięgiel P. CCL18 in the Progression of Cancer. Int J Mol Sci. 2020 Oct 26;21(21):7955.

Schraufstatter IU, Zhao M, Khaldoyanidi SK, Discipio RG. The chemokine CCL18 causes maturation of cultured monocytes to macrophages in the M2 spectrum. Immunology. 2012 Apr;135(4):287-98.

DOI: http://dx.doi.org/10.12345/yzlcyxzz.v8i8.30667