Gut microbiota transplantation drives the adoptive transfer of colonic genotype-phenotype characteristics between mice lacking catestatin and their wild type counterparts.
Gut microbiota transplantation drives the adoptive transfer of colonic genotype-phenotype characteristics between mice lacking catestatin and their wild type counterparts.
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肠道微生物群移植驱动缺乏猫蛋白的小鼠与其野生型对应物之间的结肠基因型 - 表型特征的过继转移。
DOI：
10.1080/19490976.2022.2081476
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发表时间：
2022-01
期刊：
影响因子：
12.2
通讯作者：
El Aidy, Sahar
中科院分区：
文献类型：
--
作者：
Gonzalez-Davila, Pamela;Schwalbe, Markus;Danewalia, Arpit;Wardenaar, Rene;Dalile, Boushra;Verbeke, Kristin;Mahata, Sushil K.;El Aidy, Sahar
肠道微生物群通过代谢、神经免疫和神经内分泌途径与肠黏膜持续相互作用。肠内分泌细胞（如catestatin）产生的抗菌肽水平的破坏与肠道微生物群的变化和肠道内平衡的不平衡有关。然而，肠道微生物群的变化是否在肠道失衡中起因果作用仍是一个谜。为此，我们在野生型小鼠和敲除嗜铬粒蛋白a基因catestatin编码区小鼠（CST-KO小鼠）中进行了互惠的粪便微生物移植。结合微生物群系统发育分析，RNA测序和透射电镜。从睾丸素缺乏的小鼠（CST-KO）到微生物群缺失的野生型小鼠的粪便微生物群移植诱导了受体动物扭曲结肠的转录和生理特征，包括紧密连接的损伤，以及表明结肠纤维化的胶原面积分数的增加。相比之下，将野生型小鼠的粪便微生物群移植到微生物群缺失的CST-KO小鼠中，受体CST-KO小鼠的胶原纤维化面积减少，紧密连接形态恢复，脂肪酸代谢改变。本研究全面概述了粪便微生物群移植共同介导的小鼠代谢和免疫相关细胞途径和过程，并支持肠道微生物群在小鼠结肠畸形中与睾丸素缺乏相关的突出作用。总体而言，数据表明肠道微生物群可能在肠道炎症和代谢紊乱的特征发展中发挥因果作用，已知与睾丸素水平改变有关，因此可能为治疗和预防这些疾病提供一个可控制的靶点。
The gut microbiota is in continuous interaction with the intestinal mucosa via metabolic, neuro-immunological, and neuroendocrine pathways. Disruption in levels of antimicrobial peptides produced by the enteroendocrine cells, such as catestatin, has been associated with changes in the gut microbiota and imbalance in intestinal homeostasis. However, whether the changes in the gut microbiota have a causational role in intestinal dyshomeostasis has remained elusive. To this end, we performed reciprocal fecal microbial transplantation in wild-type mice and mice with a knockout in the catestatin coding region of the chromogranin-A gene (CST-KO mice). Combined microbiota phylogenetic profiling, RNA sequencing, and transmission electron microscopy were employed. Fecal microbiota transplantation from mice deficient in catestatin (CST-KO) to microbiota-depleted wild-type mice induced transcriptional and physiological features characteristic of a distorted colon in the recipient animals, including impairment in tight junctions, as well as an increased collagen area fraction indicating colonic fibrosis. In contrast, fecal microbiota transplantation from wild-type mice to microbiota-depleted CST-KO mice reduced collagen fibrotic area, restored disrupted tight junction morphology, and altered fatty acid metabolism in recipient CST-KO mice. This study provides a comprehensive overview of the murine metabolic- and immune-related cellular pathways and processes that are co-mediated by the fecal microbiota transplantation and supports a prominent role for the gut microbiota in the colonic distortion associated with the lack of catestatin in mice. Overall, the data show that the gut microbiota may play a causal role in the development of features of intestinal inflammation and metabolic disorders, known to be associated with altered levels of catestatin and may, thus, provide a tractable target in the treatment and prevention of these disorders.
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影响因子：
48
作者：
Callahan BJ;McMurdie PJ;Rosen MJ;Han AW;Johnson AJ;Holmes SP
通讯作者：
Holmes SP
影响因子：
4.6
作者：
Earley, Helen;Lennon, Grainne;O'Connell, P. Ronan
通讯作者：
O'Connell, P. Ronan
影响因子：
8
作者：
El Aidy, Sahar;van Baarlen, Peter;Kleerebezem, Michiel
通讯作者：
Kleerebezem, Michiel
DOI：
10.1016/j.bbadis.2005.12.006
发表时间：
2006-03-01
影响因子：
6.2
作者：
Heimerl, S;Moehle, C;Schmitz, G
通讯作者：
Schmitz, G
影响因子：
1.3
作者：
Durakoğlugil ME;Ayaz T;Kocaman SA;Kırbaş A;Durakoğlugil T;Erdoğan T;Çetin M;Şahin OZ;Çiçek Y
通讯作者：
Çiçek Y