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肠上皮细胞源性白细胞介素-7:全肠外营养小鼠模型中上皮内淋巴细胞改变的一种机制。

Intestinal epithelial cell-derived interleukin-7: A mechanism for the alteration of intraepithelial lymphocytes in a mouse model of total parenteral nutrition.

作者信息

Yang Hua, Sun Xiaoyi, Haxhija Emir Q, Teitelbaum Daniel H

机构信息

Section of Pediatric Surgery, Department of Surgery, the University of Michigan Medical School and the C S Mott Children's Hospital, Ann Arbor, Michigan, USA.

出版信息

Am J Physiol Gastrointest Liver Physiol. 2007 Jan;292(1):G84-91. doi: 10.1152/ajpgi.00192.2006.

DOI:10.1152/ajpgi.00192.2006
PMID:17215438
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1773014/
Abstract

Total parenteral nutrition (TPN), with the absence of enteral nutrition, results in profound changes to both intestinal epithelial cells (EC) as well as the adjacent intraepithelial lymphocyte (IEL) population. Intestinal EC are a rich source of IL-7, a critical factor to support the maintenance of several lymphoid tissues, and TPN results in marked EC changes. On this basis, we hypothesized that TPN would diminish EC-derived IL-7 expression and that this would contribute to the observed changes in the IEL population. Mice received enteral food and intravenous crystalloid solution (control group) or TPN. TPN administration significantly decreased EC-derived IL-7 expression, along with significant changes in IEL phenotype; decreased IEL proliferation; and resulted in a marked decrease in IEL numbers. To better determine the relevance of TPN-related changes in IL-7, TPN mice supplemented with exogenous IL-7 or mice allowed ad libitum feeding and treated with exogenous administration of anti-IL-7 receptor (IL-7R) antibody were also studied. Exogenous IL-7 administration in TPN mice significantly attenuated TPN-associated IEL changes, whereas blocking IL-7R in normal mice resulted in several similar changes in IEL to those observed with TPN. These findings suggest that a decrease in EC-derived IL-7 expression may be a contributing mechanism to account for the observed TPN-associated IEL changes.

摘要

全肠外营养(TPN),在缺乏肠内营养的情况下,会导致肠上皮细胞(EC)以及相邻的上皮内淋巴细胞(IEL)群体发生深刻变化。肠EC是白细胞介素-7(IL-7)的丰富来源,IL-7是支持多种淋巴组织维持的关键因子,而TPN会导致明显的EC变化。在此基础上,我们假设TPN会减少EC衍生的IL-7表达,并且这将导致观察到的IEL群体变化。小鼠接受肠内食物和静脉晶体溶液(对照组)或TPN。给予TPN显著降低了EC衍生的IL-7表达,同时IEL表型也发生了显著变化;IEL增殖减少;并导致IEL数量显著减少。为了更好地确定TPN相关的IL-7变化的相关性,还研究了补充外源性IL-7的TPN小鼠或随意进食并接受外源性抗IL-7受体(IL-7R)抗体治疗的小鼠。在TPN小鼠中给予外源性IL-7显著减轻了与TPN相关的IEL变化,而在正常小鼠中阻断IL-7R导致IEL出现了一些与TPN观察到的相似变化。这些发现表明,EC衍生的IL-7表达降低可能是导致观察到的与TPN相关的IEL变化的一个促成机制。

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本文引用的文献

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Novel agents in the treatment of intestinal failure: humoral factors.治疗肠衰竭的新型药物:体液因子
Gastroenterology. 2006 Feb;130(2 Suppl 1):S117-21. doi: 10.1053/j.gastro.2005.08.059.
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Exogenous interleukin 7 affects gut-associated lymphoid tissue in mice receiving total parenteral nutrition.外源性白细胞介素7影响接受全胃肠外营养小鼠的肠道相关淋巴组织。
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Interleukin-7 administration alters intestinal intraepithelial lymphocyte phenotype and function in vivo.
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Keratinocyte growth factor up-regulates Interleukin-7 expression following intestinal ischemia/reperfusion in vitro and in vivo.角质形成细胞生长因子在体内外肠道缺血/再灌注后上调白细胞介素-7的表达。
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Nutrition and gut immunity.营养与肠道免疫。
Surg Clin North Am. 2011 Aug;91(4):755-70, vii. doi: 10.1016/j.suc.2011.04.007. Epub 2011 Jun 8.
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Glutamine prevents total parenteral nutrition-associated changes to intraepithelial lymphocyte phenotype and function: a potential mechanism for the preservation of epithelial barrier function.谷氨酰胺可预防肠外营养相关的上皮内淋巴细胞表型和功能改变:维持上皮屏障功能的潜在机制。
J Interferon Cytokine Res. 2010 Feb;30(2):67-80. doi: 10.1089/jir.2009.0046.
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Enteral versus parenteral nutrition: effect on intestinal barrier function.肠内营养与肠外营养:对肠道屏障功能的影响
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Therapeutic approaches to chronic intestinal inflammation by specific targeting of mucosal IL-7/IL-7R signal pathway.通过特异性靶向黏膜IL-7/IL-7R信号通路治疗慢性肠道炎症的方法。
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