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首页> 外文期刊>Allergy >IL-25 regulates the expression of adhesion molecules on eosinophils: mechanism of eosinophilia in allergic inflammation.
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IL-25 regulates the expression of adhesion molecules on eosinophils: mechanism of eosinophilia in allergic inflammation.

机译：IL-25调节嗜酸性粒细胞上粘附分子的表达：过敏性炎症中嗜酸性粒细胞的机制。

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Background: Interleukin-25 (IL-25) is a novel T-helper-2 (Th2) cytokine of the IL-17 family that plays a key role in allergic inflammation. Recent studies reported that over-expression of IL-25 in mouse induces eosinophilia. We investigated the effect of IL-25 on the expression of several adhesion molecules on human eosinophils and the underlying intracellular mechanisms. Methods: Viability of eosinophils was measured by annexin V-flourescein isothiocyanate (FITC) assay. Gene expression and surface expression of intercellular adhesion molecule (ICAM)-1 (CD54), ICAM-3 (CD50), L-selectin (CD62L), leukocyte function-associated antigen (LFA-1) (CD11a/CD18) and very late antigen-4 (VLA-4, CD49d/CD29) on eosinophils were measured by reverse transcriptase-polymerase chain reaction (RT-PCR) and flow cytometry, respectively. Adhesion of eosinophils to fibronectin was assessed using the fibronectin-coated insert system. Results: Viability of eosinophils was significantly enhanced by IL-25 from 41% to 76% dose-dependently. IL-25 could significantly upregulate the surface expression of ICAM-1, but suppress those of ICAM-3 and L-selectin on eosinophils in a dose-dependent manner. Adhesion of eosinophils to fibronectin was also significantly enhanced by IL-25. Besides, pre-incubation with p38 mitogen-activated protein kinases (MAPK) inhibitor SB203580, C-Jun NH(2)-terminal protein kinases (JNK) inhibitor SP600125 and proteosome inhibitor MG-132 could significantly restrain the effects of IL-25 on surface expression of L-selectin, ICAM-1 and ICAM-3, respectively, and also on the adhesion of eosinophils onto fibronectin (all P < 0.05). Conclusions: Our findings suggest an essential role of IL-25 in enhancing survival and regulating surface expression of ICAM-1, ICAM-3 and L-selectin on human eosinophils through the activation of p38 MAPK, JNK and nuclear factor (NF)-kappaB pathways, thereby shedding light on the molecular mechanisms of IL-25-induced eosinophilia in allergic inflammation.
机译：背景：白介素25（IL-25）是IL-17家族的新型T-helper-2（Th2）细胞因子，在变应性炎症中起关键作用。最近的研究报道，小鼠中IL-25的过表达诱导嗜酸性粒细胞增多。我们研究了IL-25对人嗜酸性粒细胞上几种粘附分子表达的影响以及潜在的细胞内机制。方法：通过膜联蛋白V-异硫氰酸荧光素（FITC）测定法测定嗜酸性粒细胞的活力。细胞间粘附分子（ICAM）-1（CD54），ICAM-3（CD50），L-选择素（CD62L），白细胞功能相关抗原（LFA-1）（CD11a / CD18）的基因表达和表面表达分别通过逆转录聚合酶链反应（RT-PCR）和流式细胞仪测量嗜酸性粒细胞上的抗原4（VLA-4，CD49d / CD29）。使用纤连蛋白包被的插入系统评估嗜酸性粒细胞对纤连蛋白的粘附。结果：IL-25使嗜酸性粒细胞的存活率从41％显着提高到76％。 IL-25可以显着上调ICAM-1的表面表达，但以剂量依赖的方式抑制嗜酸性粒细胞上ICAM-3和L-选择素的表达。 IL-25也显着增强了嗜酸性粒细胞对纤连蛋白的粘附。此外，与p38丝裂原活化蛋白激酶（MAPK）抑制剂SB203580，C-Jun NH（2）末端蛋白激酶（JNK）抑制剂SP600125和蛋白体抑制剂MG-132一起预孵育可以显着抑制IL-25对L-选择蛋白，ICAM-1和ICAM-3的表面表达，以及嗜酸性粒细胞粘附在纤连蛋白上的表达（所有P <0.05）。结论：我们的发现表明IL-25通过激活p38 MAPK，JNK和核因子（NF）-κB在提高人类嗜酸性粒细胞的存活率和调节ICAM-1，ICAM-3和L-选择素的表面表达中起着重要作用。途径，从而阐明了IL-25诱导的变应性炎症中嗜酸性粒细胞增多的分子机制。

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