Rakočević Sara, Mališ Vanja, Kozić Ljiljana, Dubovina Anđela, Drakul Marija, Bokonjić Dejan, Čolić Miodrag, Mihajlović Dušan
Faculty of Medicine Foča, University of East Sarajevo, Studentska 5, 73 300 Foča, Bosnia and Herzegovina.
Serbian Academy of Sciences and Arts, Kneza Mihajla 35, 11000 Belgrade, Serbia.
Molecules. 2024 Dec 30;30(1):113. doi: 10.3390/molecules30010113.
Dapsone is a sulfone used in treating inflammatory skin conditions. Despite its widespread dermatological use, the pharmacological actions of dapsone remain poorly understood. Here, we examined how different aspects of neutrophil functions are affected by dapsone. Peripheral blood neutrophils from healthy donors were stimulated with phorbol-12-myristate-13-acetate (PMA), N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP), or calcium ionophore (CaI) or primed with cytokines prior to stimulation, in the presence of different concentrations of dapsone (from 10 to 50 µg/mL), followed by analyses of their survival, phenotype, and functional properties. We found that dapsone at the concentration of 50 μg/mL induced a significant neutrophil apoptotic rate during 6 h and 18 h, while other concentrations were well tolerated compared to control non-treated cells. However, dapsone significantly decreased the induced oxidative burst of neutrophils at all non-cytotoxic concentrations. Additionally, dapsone showed a dose-dependent suppression of NETosis in activated neutrophils. The production of IL-8 by dapsone-treated neutrophils was decreased under both stimulated (fMLP) and primed (TNF-α/fMLP) conditions. Moreover, dapsone inhibited the expression of CD11b/CD18, CD66, and CD89 and reversed or significantly mitigated the downregulation of CD16, CD32, CD181, CD88, and CD62L on neutrophils after priming and fMLP stimulation. In conclusion, our results indicate the complexity of dapsone actions on neutrophil functions, extending previous knowledge on the suppression of oxidative burst and IL-8 production upon neutrophils' activation. Suppressed NETosis and modulation of marker expression associated with different neutrophil functions under inflammatory conditions are new findings, not recognized previously.
氨苯砜是一种用于治疗炎症性皮肤病的砜类药物。尽管其在皮肤科广泛应用,但其药理作用仍知之甚少。在此,我们研究了氨苯砜如何影响中性粒细胞功能的不同方面。在不同浓度(10至50μg/mL)的氨苯砜存在下,用佛波醇-12-肉豆蔻酸酯-13-乙酸酯(PMA)、N-甲酰-L-蛋氨酰-L-亮氨酰-L-苯丙氨酸(fMLP)或钙离子载体(CaI)刺激健康供体的外周血中性粒细胞,或在刺激前用细胞因子进行预处理,随后分析其存活、表型和功能特性。我们发现,50μg/mL浓度的氨苯砜在6小时和18小时诱导了显著的中性粒细胞凋亡率,而与未处理的对照细胞相比,其他浓度的氨苯砜耐受性良好。然而,在所有非细胞毒性浓度下,氨苯砜显著降低了中性粒细胞诱导的氧化爆发。此外,氨苯砜对活化的中性粒细胞中的中性粒细胞胞外陷阱形成呈剂量依赖性抑制。在刺激(fMLP)和预处理(TNF-α/fMLP)条件下,经氨苯砜处理的中性粒细胞产生的IL-8均减少。此外,氨苯砜抑制CD11b/CD18、CD66和CD89的表达,并逆转或显著减轻预处理和fMLP刺激后中性粒细胞上CD16、CD32、CD181、CD88和CD62L的下调。总之,我们的结果表明氨苯砜对中性粒细胞功能作用的复杂性,扩展了先前关于中性粒细胞活化时氧化爆发和IL-8产生受抑制的认识。炎症条件下中性粒细胞胞外陷阱形成受抑制以及与不同中性粒细胞功能相关标志物表达的调节是新发现,以前未被认识到。