Gomułka Krzysztof, Liebhart Jerzy, Jaskuła Emilia, Mędrala Wojciech
Department of Internal Medicine, Pneumology and Allergology, Wroclaw Medical University, Wroclaw, Poland.
Emeritus Professor, Department of Internal Medicine, Pneumology and Allergology, Wroclaw Medical University, Wroclaw, Poland.
Postepy Dermatol Alergol. 2022 Apr;39(2):275-280. doi: 10.5114/ada.2022.115888. Epub 2022 May 9.
Asthma is a complex syndrome associated with heterogeneity in the type of inflammation that modulates airway hyperresponsiveness and remodelling. Airway inflammation with neutrophils, cytokines like vascular endothelial growth factor (VEGF) and various gene polymorphisms might be relevant for asthma pathogenesis.
To investigate the expression of CD69 and CD11b markers on peripheral neutrophils after VEGF stimulation in asthmatics. Furthermore, the possible influence of a genetic factor (del/ins genotype at -2549 -2567 position in the VEGF-promoter gene) was taken into account.
122 subjects (82 asthmatics and 40 controls) participated in our study. CD69 and CD11b presence on peripheral blood neutrophils was detected using the flow cytometric method without exogenous stimulation (negative control), after N-formyl-methionine-leucyl-phenylalanine stimulation (fMLP - positive control) and after VEGF stimulation. Genotyping for the VEGF-promoter region was performed by polymerase chain reaction (PCR).
Peripheral neutrophil stimulation with VEGF enhances the activity of these cells and induces CD69 and CD11b expression in a dose-dependent manner compared with unstimulated neutrophils ( > 0.05). CD69 and CD11b markers were slightly presented ( = 0.05 and = 0.07, respectively) on neutrophils stimulated with fMLP in asthmatics with the ins genotype variant in the VEGF-promoter region.
Our results demonstrate that VEGF might insignificantly activate neutrophils in asthmatics. In addition, the modulated expression of CD69 and CD11b on peripheral neutrophils is not related to potential contribution of the VEGF gene polymorphism.
哮喘是一种复杂的综合征,与调节气道高反应性和重塑的炎症类型的异质性有关。伴有中性粒细胞的气道炎症、血管内皮生长因子(VEGF)等细胞因子以及各种基因多态性可能与哮喘发病机制相关。
研究哮喘患者经VEGF刺激后外周血中性粒细胞上CD69和CD11b标志物的表达。此外,还考虑了一个遗传因素(VEGF启动子基因-2549至-2567位的缺失/插入基因型)的可能影响。
122名受试者(82名哮喘患者和40名对照)参与了我们的研究。使用流式细胞术在无外源性刺激(阴性对照)、N-甲酰甲硫氨酸-亮氨酰-苯丙氨酸刺激(fMLP-阳性对照)和VEGF刺激后检测外周血中性粒细胞上CD69和CD11b的存在情况。通过聚合酶链反应(PCR)对VEGF启动子区域进行基因分型。
与未刺激的中性粒细胞相比,用VEGF刺激外周血中性粒细胞可增强这些细胞的活性,并以剂量依赖方式诱导CD69和CD11b表达(>0.05)。在VEGF启动子区域具有插入基因型变体的哮喘患者中,用fMLP刺激的中性粒细胞上CD69和CD11b标志物略有表达(分别为=0.05和=0.07)。
我们的结果表明,VEGF可能对哮喘患者的中性粒细胞有轻微激活作用。此外,外周血中性粒细胞上CD69和CD11b的调节表达与VEGF基因多态性的潜在作用无关。