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首页> 外文期刊>American Journal of Physiology >Interleukin-4- and -13-induced hypercontractility of human intestinal muscle cells-implication for motility changes in Crohn's disease.
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Interleukin-4- and -13-induced hypercontractility of human intestinal muscle cells-implication for motility changes in Crohn's disease.

机译：白细胞介素4和-13诱导的人肠道肌肉细胞过度收缩-暗示克罗恩病的运动性改变。

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摘要

Crohn's disease is an idiopathic inflammatory condition. However, little is known about the changes that occur in the muscularis externa, despite the fact that this tissue contributes to motility changes and stricture formation. We characterized immune activity in the muscularis externa from intestinal segments of Crohn's disease patients and evaluated the role of IL-4 and -13 as well as signal transducer and activator of transcription (STAT)6 in the contractility of the cultured human intestinal smooth muscle cells. CD3+ve cells (P < 0.01) and IL-4 protein (P < 0.01) were significantly increased in the muscularis externa of Crohn's disease patients compared with noninflamed controls. Preincubation of human cultured smooth muscle cells with IL-4 (P < 0.001) or IL-13 (P < 0.05) significantly enhanced carbachol-induced contraction, and this was significantly inhibited by the STAT6 inhibitor leflunomide (P < 0.0001). A similar profile was observed in muscle cells isolated from Crohn's disease patients. Both IL-4 and IL-13 increased specific STAT6-DNA binding in control cells, and this was inhibited by anti-STAT6 Ab (P < 0.05) or leflunomide (P < 0.05). IL-4 and IL-13 mediate the hypercontractility of intestinal muscle via a STAT6 pathway at the level of the smooth muscle cell. The STAT6 pathway may contribute to the hypercontractility of intestinal muscle in Crohn's disease.
机译：克罗恩病是一种特发性炎症。但是，尽管该组织有助于运动性改变和狭窄形成，但鲜为人知在外部肌层中发生的改变。我们表征了克罗恩病患者肠段的外肌层的免疫活性，并评估了IL-4和-13以及信号转导和转录激活因子（STAT）6在培养的人肠平滑肌细胞收缩性中的作用。与非发炎对照相比，克罗恩病患者的肌外肌中CD3 + ve细胞（P <0.01）和IL-4蛋白（P <0.01）显着增加。用IL-4（P <0.001）或IL-13（P <0.05）对人培养的平滑肌细胞进行预培养显着增强了卡巴胆碱引起的收缩，而STAT6抑制剂来氟米特显着抑制了收缩（P <0.0001）。从克罗恩氏病患者分离的肌肉细胞中观察到相似的情况。 IL-4和IL-13均增加了对照细胞中的特定STAT6-DNA结合，并且被抗STAT6 Ab（P <0.05）或来氟米特（P <0.05）抑制。 IL-4和IL-13通过STAT6途径在平滑肌细胞水平介导肠道肌肉的过度收缩。 STAT6途径可能在克罗恩病中促进肠道肌肉的过度收缩。

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