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白细胞介素-17通过核因子κB和丝裂原活化蛋白激酶途径刺激人结肠肌成纤维细胞的炎症反应。

IL-17 stimulates inflammatory responses via NF-kappaB and MAP kinase pathways in human colonic myofibroblasts.

作者信息

Hata Kazunori, Andoh Akira, Shimada Mitsue, Fujino Sanae, Bamba Shigeki, Araki Yoshio, Okuno Takafumi, Fujiyama Yoshihide, Bamba Tadao

机构信息

Department of Internal Medicine, Shiga University of Medical Science, Seta-Tsukinowa, Otsu 520-2192, Japan.

出版信息

Am J Physiol Gastrointest Liver Physiol. 2002 Jun;282(6):G1035-44. doi: 10.1152/ajpgi.00494.2001.

Abstract

Colonic subepithelial myofibroblasts (SEMFs) may play a role in the modulation of mucosal inflammatory responses. We investigated the effects of interleukin (IL)-17 on IL-6 and chemokine [IL-8 and monocyte chemoattractant protein (MCP)-1] secretion in colonic SEMFs. Cytokine expression was determined by ELISA and Northern blotting. Nuclear factor kappa B (NF-kappaB) DNA-binding activity was evaluated by electrophortetic gel mobility shift assay (EMSA). The activation of mitogen-activated protein kinase (MAPK) was assessed by immunoblotting. IL-6, IL-8, and MCP-1 secretions were rapidly induced by IL-17. IL-17 induced NF-kappaB activation within 45 min after stimulation. A blockade of NF-kappaB activation markedly reduced these responses. MAPK inhibitors (SB-203580, PD-98059, and U-0126) significantly reduced the IL-17-induced IL-6 and chemokine secretion. The combination of either IL-17 + IL-1beta or IL-17 + tumor necrosis factor (TNF)-alpha enhanced cytokine secretion; in particular, the effects of IL-17 + TNF-alpha on IL-6 secretion were much stronger than the other responses. This was dependent on the enhancement of IL-6 mRNA stability. In conclusion, human SEMFs secreted IL-6, IL-8, and MCP-1 in response to IL-17. These responses might play an important role in the pathogenesis of gut inflammation.

摘要

结肠上皮下肌成纤维细胞(SEMFs)可能在调节黏膜炎症反应中发挥作用。我们研究了白细胞介素(IL)-17对结肠SEMFs中IL-6和趋化因子[IL-8和单核细胞趋化蛋白(MCP)-1]分泌的影响。通过酶联免疫吸附测定(ELISA)和Northern印迹法测定细胞因子表达。通过电泳凝胶迁移率变动分析(EMSA)评估核因子κB(NF-κB)的DNA结合活性。通过免疫印迹法评估丝裂原活化蛋白激酶(MAPK)的激活情况。IL-17可迅速诱导IL-6、IL-8和MCP-1的分泌。IL-17在刺激后45分钟内诱导NF-κB激活。阻断NF-κB激活可显著降低这些反应。MAPK抑制剂(SB-203580、PD-98059和U-0126)可显著降低IL-17诱导的IL-6和趋化因子分泌。IL-17 + IL-1β或IL-17 +肿瘤坏死因子(TNF)-α的组合可增强细胞因子分泌;特别是,IL-17 + TNF-α对IL-6分泌的作用比其他反应要强得多。这取决于IL-6 mRNA稳定性的增强。总之,人SEMFs对IL-17作出反应分泌IL-6、IL-8和MCP-1。这些反应可能在肠道炎症的发病机制中起重要作用。

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