Exclusive Enteral Nutrition Alleviates Th17-Mediated Inflammation via Eliminating Mechanical Stress-Induced Th17-Polarizing Cytokines in Crohn's-like Colitis.
Exclusive Enteral Nutrition Alleviates Th17-Mediated Inflammation via Eliminating Mechanical Stress-Induced Th17-Polarizing Cytokines in Crohn's-like Colitis.
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独家肠内营养通过消除克罗恩病样结肠炎中机械应力诱导的 Th17 极化细胞因子来减轻 Th17 介导的炎症。
DOI：
10.1093/ibd/izad158
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发表时间：
2024
影响因子：
4.9
通讯作者：
Shi,Xuan-Zheng
中科院分区：
文献类型：
--
作者：
Geesala,Ramasatyaveni;Zhang,Ke;Lin,You-Min;Johnson,JohnC;Cong,Yingzi;Cohn,Steven;Shi,Xuan-Zheng
背景和目的单纯肠内营养（EEN）加流质饮食是克罗恩病（CD）唯一确定的饮食治疗方法。然而，EEN在CD中的作用机制尚不清楚。辅助性T细胞17（Th 17）免疫应答在CD中起关键作用。我们假设EEN通过消除机械应力诱导的Th 17极化cytokines.MethodsA大鼠克罗恩样结肠炎模型的表达增强了Th 17反应，通过结肠内滴注TNBS（65 mg/kg，溶于250 µL 40%乙醇中）建立。对照组大鼠用生理盐水处理。我们的特点是免疫表型和分子的变化，在控制和结肠炎大鼠与EEN治疗和不治疗。Th 17分化确定使用cocultureassays.ResultsTNBS滴注诱导透壁炎症与狭窄的炎症部位和一个显着增加的Th 17极化细胞因子白细胞介素（IL）-6和骨桥蛋白和Th 17细胞群在机械膨胀的炎症前的网站（P-网站）。EEN治疗消除了机械扩张和P部位IL-6、骨桥蛋白和Th 17反应的增加。IL-6和骨桥蛋白主要表达于外肌层。体外机械牵拉结肠平滑肌细胞可诱导IL-6和骨桥蛋白的大量增加。当幼稚T细胞与来自P位点组织或拉伸细胞的条件培养基一起培养时，Th 17分化显著增加。IL-6的抑制，但不删除骨桥蛋白，阻止了增加的Th 17 differentiation.ConclusionsMechanical stress诱导Th 17极化细胞因子在结肠。EEN通过消除克罗恩样结肠炎中机械应激诱导的IL-6来减弱Th 17免疫应答
Background and AimsExclusive enteral nutrition (EEN) with a liquid diet is the only established dietary treatment for Crohn’s’ disease (CD). However, the mechanism of action of EEN in CD is unclear. T helper 17 (Th17) immune response plays a critical role in CD. We hypothesized that EEN alleviates Th17 response by eliminating mechanical stress–induced expression of Th17-polarizing cytokines.MethodsA rat model of Crohn’s-like colitis was established by intracolonic instillation of TNBS (65 mg/kg in 250 µL of 40% ethanol). Control rats were treated with saline. We characterized immunophenotypes and molecular changes of the colon in control and colitis rats with and without EEN treatment. Th17 differentiation was determined using coculture assays.ResultsTNBS instillation induced transmural inflammation with stenosis in the inflammation site and a marked increase of Th17-polarizing cytokines interleukin (IL)-6 and osteopontin and the Th17 cell population in the mechanically distended preinflammation site (P-site). EEN treatment eliminated mechanical distention and the increase of IL-6, osteopontin, and Th17 response in the P-site. IL-6 and osteopontin expression was found mainly in the muscularis externa. Mechanical stretch of colonic smooth muscle cells in vitro induced a robust increase of IL-6 and osteopontin. When naïve T cells were cultured with conditioned media from the P-site tissue or stretched cells, Th17 differentiation was significantly increased. Inhibition of IL-6, but not deletion of osteopontin, blocked the increase of Th17 differentiation.ConclusionsMechanical stress induces Th17-polarizing cytokines in the colon. EEN attenuates Th17 immune response by eliminating mechanical stress–induced IL-6 in Crohn’s-like colitis.
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DOI：
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期刊：
The Journal of biological chemistry
影响因子：
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