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潘氏细胞与肠道微生物群研究中涉及的关键设计方面。

Critical design aspects involved in the study of Paneth cells and the intestinal microbiota.

作者信息

Shanahan Michael T, Carroll Ian M, Gulati Ajay S

机构信息

Department of Medicine; Division of Gastroenterology and Hepatology; University of North Carolina at Chapel Hill; Chapel Hill, NC USA.

Department of Pediatrics; Division of Gastroenterology; University of North Carolina at Chapel Hill; Chapel Hill, NC USA.

出版信息

Gut Microbes. 2014 Mar-Apr;5(2):208-14. doi: 10.4161/gmic.27466. Epub 2013 Dec 20.

DOI:10.4161/gmic.27466
PMID:24637592
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4063846/
Abstract

Paneth cells are long-lived secretory cells that reside in the base of the crypts of Lieberkühn of the small intestine. They produce an arsenal of molecules that are involved in numerous biological processes, ranging from the control of gut microbial populations to supporting the intestinal stem cell niche. Because of these important functions, Paneth cell abnormalities are becoming implicated in a variety of disease processes. As such, it is necessary to establish parameters that will allow for the comprehensive study of Paneth cells in health and disease. In this addendum, we highlight critical design aspects involved in the study of Paneth cells and their downstream effects on the intestinal microbiota. The importance of this approach is demonstrated by our recent findings that Nod2 does not regulate mouse Paneth cell antimicrobial function, in contrast to previous reports. This work defines key issues to consider when studying Paneth cells in mouse systems.

摘要

潘氏细胞是一种长寿的分泌细胞,位于小肠利伯库恩隐窝的底部。它们产生一系列分子,这些分子参与众多生物过程,从控制肠道微生物群落到支持肠道干细胞生态位。由于这些重要功能,潘氏细胞异常正被认为与多种疾病过程有关。因此,有必要建立一些参数,以便对健康和疾病状态下的潘氏细胞进行全面研究。在本附录中,我们强调了潘氏细胞研究及其对肠道微生物群下游影响所涉及的关键设计方面。我们最近的研究结果表明,与之前的报道相反,Nod2并不调节小鼠潘氏细胞的抗菌功能,这一方法的重要性由此得到了证明。这项工作定义了在小鼠系统中研究潘氏细胞时需要考虑的关键问题。

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本文引用的文献

1
Paneth cells as a site of origin for intestinal inflammation.潘氏细胞作为肠道炎症的起源部位。
Nature. 2013 Nov 14;503(7475):272-6. doi: 10.1038/nature12599. Epub 2013 Oct 2.
2
Irgm1-deficient mice exhibit Paneth cell abnormalities and increased susceptibility to acute intestinal inflammation.Irgm1 缺陷小鼠表现出潘氏细胞异常和对急性肠道炎症的易感性增加。
Am J Physiol Gastrointest Liver Physiol. 2013 Oct 15;305(8):G573-84. doi: 10.1152/ajpgi.00071.2013. Epub 2013 Aug 29.
3
Stochastic changes over time and not founder effects drive cage effects in microbial community assembly in a mouse model.时间上的随机变化而非奠基者效应驱动了小鼠模型中微生物群落组装的笼效应。
ISME J. 2013 Nov;7(11):2116-25. doi: 10.1038/ismej.2013.106. Epub 2013 Jul 4.
4
Paneth cell marker CD24 in NOD2 knockout organoids and in inflammatory bowel disease (IBD).NOD2基因敲除类器官及炎症性肠病(IBD)中的潘氏细胞标志物CD24
Gut. 2015 Feb;64(2):353-4. doi: 10.1136/gutjnl-2013-305077. Epub 2013 May 23.
5
Nod1 and Nod2 signaling does not alter the composition of intestinal bacterial communities at homeostasis.Nod1 和 Nod2 信号通路在肠道稳态中并不改变肠道细菌群落的组成。
Gut Microbes. 2013 May-Jun;4(3):222-31. doi: 10.4161/gmic.24373. Epub 2013 Apr 2.
6
Mouse Paneth cell antimicrobial function is independent of Nod2.小鼠潘氏细胞抗菌功能不依赖于 Nod2。
Gut. 2014 Jun;63(6):903-10. doi: 10.1136/gutjnl-2012-304190. Epub 2013 Mar 19.
7
NOD2-mediated dysbiosis predisposes mice to transmissible colitis and colorectal cancer.NOD2 介导的菌群失调使小鼠易患传染性结肠炎和结直肠癌。
J Clin Invest. 2013 Feb;123(2):700-11. doi: 10.1172/JCI62236. Epub 2013 Jan 2.
8
Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease.宿主-微生物相互作用塑造了炎症性肠病的遗传结构。
Nature. 2012 Nov 1;491(7422):119-24. doi: 10.1038/nature11582.
9
Familial transmission rather than defective innate immunity shapes the distinct intestinal microbiota of TLR-deficient mice.家族遗传而非固有免疫缺陷决定 TLR 缺陷型小鼠肠道菌群的独特性。
J Exp Med. 2012 Jul 30;209(8):1445-56. doi: 10.1084/jem.20120504. Epub 2012 Jul 23.
10
Mouse background strain profoundly influences Paneth cell function and intestinal microbial composition.小鼠背景品系极大地影响潘氏细胞功能和肠道微生物组成。
PLoS One. 2012;7(2):e32403. doi: 10.1371/journal.pone.0032403. Epub 2012 Feb 27.