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首页> 外文期刊>Neurogastroenterology and motility >Rat enteric glial cells express novel isoforms of Interleukine-7 regulated during inflammation
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Rat enteric glial cells express novel isoforms of Interleukine-7 regulated during inflammation

机译：大鼠肠道胶质细胞表达在炎症期间调节的新型异种血荷母素-7的新型同种型

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Background Neuroimmune interactions are essential to maintain gut homeostasis and prevent intestinal disorders but so far, the impact of enteric glial cells (EGC) on immune cells remains a relatively unexplored area of research. As a dysregulation of critical cytokines such as interleukine-7 (IL-7) was suggested to exacerbate gut chronic inflammation, we investigated whether EGC could be a source of IL-7 in the gastrointestinal tract. Methods Expression of IL-7 in the rat enteric nervous system was analyzed by immunochemistry and Q-PCR. IL-7 variants were cloned and specific antibodies against rat IL-7 isoforms were raised to characterize their expression in the submucosal plexus. IL-7 isoforms were produced in vitro to analyze their impact on T-cell survival. Key Results Neurons and glial cells of the rat enteric nervous system expressed IL-7 at both mRNA and protein levels. Novel rat IL-7 isoforms with distinct C-terminal parts were detected. Three of these isoforms were found in EGC or in both enteric neurons and EGC. Exposure of EGC to pro-inflammatory cytokines (IL-1 beta and/or TNF alpha) induced an upregulation of all IL-7 isoforms. Interestingly, time-course and intensity of the upregulation varied according to the presence or absence of exon 5a in IL-7 variants. Functional analysis on T lymphocytes revealed that only canonical IL-7 protects T cells from cell death. Conclusions and Inferences IL-7 and its variants are expressed by neurons and glial cells in the enteric nervous system. Their distinct expression and upregulation in inflammatory conditions suggest a role in gut homeostasis which could be critical in case of chronic inflammatory diseases.
机译：背景技术神经免疫相互作用对于维持肠道稳态并预防肠道障碍，但到目前为止，肠道胶质细胞（EGC）对免疫细胞的影响仍然是一个相对未开发的研究领域。作为表达细胞因子的疑难解理，例如白细胞血管素-7（IL-7），提示加剧肠道慢性炎症，我们研究了EGC是否可以是胃肠道中IL-7的来源。方法通过免疫化学和Q-PCR分析了大鼠肠道神经系统中IL-7的表达。克隆IL-7变体并升高对大鼠IL-7同种型的特异性抗体，以表征其在粘膜丛中的表达。体外生产IL-7同种型，分析它们对T细胞存活的影响。关键结果是大鼠肠道神经系统的神经元和胶质细胞在mRNA和蛋白质水平中表达IL-7。检测到具有不同C末端部件的新型大鼠IL-7同种型。在EGC或肠道神经元和EGC中发现了三种同种型。 EGC暴露于促炎细胞因子（IL-1β和/或TNFα）诱导所有IL-7同种型的上调。有趣的是，上调的时间过程和强度根据IL-7变体中的外显子5A的存在或不存在而变化。 T淋巴细胞功能分析显示，只有规范IL-7只能保护T细胞免受细胞死亡。结论和推迟IL-7及其变体由神经元和肠道神经系统中的神经元和胶质细胞表达。它们在炎症病症中的明显表达和上调表明，在肠道稳态中的作用可能是慢性炎症疾病的关键。

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