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首页> 外文期刊>Cellular Signalling >Tumor necrosis factor-alpha (TNF-alpha) induces integrin CD11b/CD18 (Mac-1) up-regulation and migration to the CC chemokine CCL3 (MIP-1 alpha) on human neutrophils through defined signalling pathways
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Tumor necrosis factor-alpha (TNF-alpha) induces integrin CD11b/CD18 (Mac-1) up-regulation and migration to the CC chemokine CCL3 (MIP-1 alpha) on human neutrophils through defined signalling pathways

机译：肿瘤坏死因子-α（TNF-α）诱导整联蛋白CD11b / CD18（Mac-1）上调并通过确定的信号通路迁移至人中性粒细胞的CC趋化因子CCL3（MIP-1 alpha）

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Strong evidence suggests that neutrophils may play an active role in acute and chronic inflammatory disorders, such as rheumatoid arthritis and atherosclerosis. Given the role of pro-inflammatory cytokine TNF-alpha in these inflammatory processes, we planned the present study to investigate the effect of short term incubation with TNF-alpha on neutrophil migration to CCL3, a chemokine produced in inflammatory sites and normally devoid of neutrophil chemotactic properties. We found that TNF-alpha primed neutrophils for migration to CCL3 via CCR5. TNF-alpha-induced migration was a consequence of the TNF-alpha-induced up-regulation of integrin CD11b/CD18 (Mac-1) on neutrophil surface. Furthermore, TNF-alpha activity was found to be strictly dependent on the activation of ERK 1/2 p44, cooperating with the intracellular pathways involving Src kinases, PI3K/Akt, p38 MAPK, well known as activated in response to classical chemoattractants (CXCL8) or priming agents (GM-CSF). On the contrary, the effect of TNF-alpha on neutrophil migration to CCL3 was not dependent on JNK 1/2. In conclusion, the present report shows that TNF-alpha unveils a previously unknown capacity of neutrophils to migrate to CCL3 through the intervention of Mac-1. TNF-alpha regulates Mac-1 up-regulation through signalling pathways, involving various kinases, but not JNK 1/2. Although highly speculative, ERK 1/2 p44 may represent a selective target for the pharmacologic manipulation of neutrophil-mediated adverse activities in TNF-alpha-mediated inflammatory states. (C) 2007 Elsevier Inc. All rights reserved.
机译：有力的证据表明，中性粒细胞可能在类风湿性关节炎和动脉粥样硬化等急性和慢性炎症性疾病中发挥积极作用。考虑到促炎细胞因子TNF-α在这些炎症过程中的作用，我们计划进行本研究，以研究与TNF-α短期孵育对嗜中性白细胞向CCL3迁移的影响，CCL3是在炎症部位产生的趋化因子，通常不含嗜中性白细胞趋化性质。我们发现TNF-α引发嗜中性粒细胞通过CCR5迁移到CCL3。 TNF-α诱导的迁移是TNF-α诱导的嗜中性粒细胞表面整联蛋白CD11b / CD18（Mac-1）上调的结果。此外，发现TNF-α活性严格依赖于ERK 1/2 p44的激活，并与涉及Src激酶，PI3K / Akt，p38 MAPK的细胞内途径协同作用，众所周知，其对经典趋化因子（CXCL8）有反应或引发剂（GM-CSF）。相反，TNF-α对嗜中性白细胞向CCL3迁移的影响并不取决于JNK 1/2。总之，本报告显示，TNF-α揭示了嗜中性粒细胞通过Mac-1干预迁移至CCL3的未知能力。 TNF-α通过信号途径调节Mac-1的上调，涉及各种激酶，但不涉及JNK 1/2。尽管高度推测，ERK 1/2 p44可能代表在TNF-α介导的炎症状态下中性粒细胞介导的不良活动的药理处理的选择性靶点。 （C）2007 Elsevier Inc.保留所有权利。

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