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首页> 外文期刊>Cytokine >Interleukin 17A evoked mucosal damage is attenuated by cannabidiol and anandamide in a human colonic explant model
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Interleukin 17A evoked mucosal damage is attenuated by cannabidiol and anandamide in a human colonic explant model

机译：白细胞介素17a诱发的粘膜损伤是由人结肠蛋白质模型中的大麻蛋白和anandamide衰减

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摘要

Interleukin 17A (IL-17A) is a cytokine linked to inflammatory bowel disease. We investigated IL-17A expression in human colonic mucosa, whether IL-17A can elicit colonic mucosal damage in a human explant model and modulate gastrointestinal epithelial permeability in cell culture. We also tested if select cannabinoid ligands, shown to be protective in colitis models could attenuate damage caused by IL-17A. In addition, the ability of pro-inflammatory cytokines TNF-α and IL-1β to modulate levels of IL-17A in the explant colitis model was also explored. IL-17A incubation caused significant mucosal epithelial and crypt damage which were attenuated following hydrocortisone treatment, and also reduced following anandamide or cannabidiol incubation. IL-17A-evoked mucosal damage was also associated with an increase in matrix metalloprotease activity. However, IL-17A did not induce any significant changes in epithelial permeability in confluent Caco-2 cell monolayers over a 48. h incubation period. IL-17A was located predominantly in human mucosal epithelium together with IL-17C, but both IL-17A and IL-17C were also expressed in the lamina propria and submucosa. Incubation of human colonic mucosal tissue or Caco-2 cells with pro-inflammatory cytokines TNF-α and IL-1β however did not alter IL-17A expression. These results indicate IL-17A has a widespread distribution in the human colon and the capacity to elicit mucosal damage which can be attenuated by cannabinoid ligands.
机译：白细胞介素17A（IL-17A）是与炎性肠病有关的细胞因子。我们研究了IL-17A在人结肠粘膜中的表达，IL-17A是否可以在人类分泌蛋白模型中引发结肠粘膜损伤并调节细胞培养中的胃肠天性上皮渗透性。我们还测试了选择大麻素配体，显示在结肠炎模型中是保护性的，可以衰减由IL-17A引起的损伤。此外，还探讨了促炎细胞因子TNF-α和IL-1β在外植体结肠炎模型中调节IL-17a水平的能力。 IL-17A孵育引起了氢化胞蔻体处理后衰减的显着粘膜上皮和隐窝损伤，并且在酰胺或大麻孵育后也减少。 IL-17A诱发的粘膜损伤也与基质金属蛋白酶的增加有关。然而，IL-17a在48℃下没有诱导融合的Caco-2细胞单层上皮渗透性的任何显着变化。 IL-17A主要位于人粘膜上皮，与IL-17C一起，但IL-17A和IL-17C也在层胶和粘膜下表达。然而，用促炎细胞因子TNF-α和IL-1β孵育人结肠粘膜组织或Caco-2细胞并未改变IL-17a表达。这些结果表明IL-17A在人性结肠中具有广泛的分布，并且可以通过大麻素配体衰减的引发粘膜损伤的能力。

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  • 来源
    《Cytokine》 |2014年第2期|共9页
  • 作者

    HarveyB.S.; SiaT.C.; WattchowD.A.; SmidS.D.;

  • 作者单位

    Discipline of Pharmacology School of Medical Sciences Faculty of Health Sciences The University;

    Department of Surgery Flinders Medical Centre Bedford Park Australia;

    Department of Surgery Flinders Medical Centre Bedford Park Australia;

    Discipline of Pharmacology School of Medical Sciences Faculty of Health Sciences The University;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    Anandamide; Cannabidiol; Colitis; Epithelial permeability; Interleukin 17;

    机译：anandamide;cannabidiol;结肠炎;上皮渗透性;白细胞介素17;

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