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首页> 外文期刊>Journal of Cellular Physiology >Inflammation Controls Sensitivity of Human and Mouse Intestinal Epithelial Cells to Galectin-1
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Inflammation Controls Sensitivity of Human and Mouse Intestinal Epithelial Cells to Galectin-1

机译：人类和炎症控制灵敏度Galectin-1小鼠肠上皮细胞

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摘要

Galectins play key roles in the inflammatory cascade. In this study, we aimed to analyze the effect of galectin-1 (Gal-1) in the function of intestinal epithelial cells (IECs) isolated from healthy and inflamed mucosa. IECs isolated from mice or patients with inflammatory bowel diseases (IBD) were incubated with different pro-inflammatory cytokines, and Gal-1 binding, secretion of homeostatic factors and viability were assessed. Experimental models of food allergy and colitis were used to evaluate the in vivo influence of inflammation on Gal-1 binding and modulation of IECs. We found an enhanced binding of Gal-1 to: (a) murine IECs exposed to IL-1, TNF, and IL-13; (b) IECs from inflamed areas in intestinal tissue from IBD patients; (c) small bowel of allergic mice; and (d) colon from mice with experimental colitis. Our results showed that low concentrations of Gal-1 favored a tolerogenic micro-environment, whereas high concentrations of this lectin modulated viability of IECs through mechanisms involving activation of caspase-9 and modulation of Bcl-2 protein family members. Our results showed that, when added in the presence of diverse pro-inflammatory cytokines such as tumor necrosis factor (TNF), IL-13 and IL-5, Gal-1 differentially promoted the secretion of growth factors including thymic stromal lymphopoietin (TSLP), epidermal growth factor (EGF), IL-10, IL-25, and transforming growth factor (TGF-(1)). In conclusion, we found an augmented binding of Gal-1 to IECs when exposed in vitro or in vivo to inflammatory stimuli, showing different effects depending on Gal-1 concentration. These findings highlight the importance of the inflammatory micro-environment of mucosal tissues in modulating IECs susceptibility to the immunoregulatory lectin Gal-1 and its role in epithelial cell homeostasis. J. Cell. Physiol. 231: 1575-1585, 2016. (c) 2015 Wiley Periodicals, Inc.
机译：Galectins炎症中扮演关键角色级联。galectin-1效果(Gal-1)的功能肠上皮细胞(iec)隔绝健康和粘膜发炎。老鼠或炎性肠道疾病患者(IBD)与不同的孵化促炎细胞因子,Gal-1绑定,分泌的自我平衡的因素和可行性被评估。过敏和结肠炎被用来评估体内炎症对Gal-1绑定和iec调制。结合Gal-1: (a)小鼠iec暴露il - 1、TNF和IL-13;地区从IBD患者肠道组织;过敏小鼠的小肠;小鼠实验性结肠炎。表明低浓度Gal-1青睐耐受性微环境,而高凝集素的浓度调制生存能力iec的激活机制caspase-9和调制的bcl - 2蛋白家庭成员。添加不同的促炎症的存在细胞因子如肿瘤坏死因子(TNF),IL-13 IL-5, Gal-1差异促进了分泌生长因子包括胸腺基质淋巴生成素(简称TSLP),表皮生长因子(EGF)、il - 10 IL-25和转换生长因子(TGF -(1))。一个增广Gal-1 iec当绑定暴露在体外或体内炎症刺激,显示不同的效果取决于Gal-1浓度。炎症微环境的重要性调制iec的粘膜组织对免疫调节外源凝集素在上皮细胞Gal-1及其作用体内平衡。2016.

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