加州大学旧金山分校的Ajay Chawla研究组发现CD11c细胞通过感知营养来改变肠道菌群从而影响食物摄入与体重。相关论文于2019年8月发表于国际学术期刊《细胞—代谢》上。

研究人员发现遗传敲除CD11c阳性髓样细胞(来自Tsc1 f/fCD11c Cre小鼠)中的Tsc1基因降低了无代谢疾病小鼠的食物摄入量和体重。共饲养和粪便移植实验表明，健康的肠道微生物群体在调节体重方面起着主导作用。16S rRNA测序、选择性培养和重组实验进一步证实，约氏乳杆菌（Lactobacillus johnsonii）Q1-7的选择性缺失导致Tsc1 f/fCD11c Cre小鼠的食物摄入量和体重下降。在机制上，CD11c细胞中mTORC1信号的激活调节约氏乳杆菌Q1-7特异IgA的产生，使其在肠道内稳定定植。总之，他们的发现揭示了一个意想不到的跨界免疫-微生物群体反馈回路，从而对哺乳动物的食物摄入量和体重进行稳态调控。

据介绍，微生物失调和炎症与饮食引起的肥胖和胰岛素抵抗有关。然而，目前还不清楚免疫力和微生物群体之间的相互作用是否也能调节健康动物的代谢稳态。
 

附：英文原文

Title: Nutrient Sensing in CD11c Cells Alters the Gut Microbiota to Regulate Food Intake and Body Mass

Author: D. Nyasha Chagwedera, Qi Yan Ang, Jordan E. Bisanz, Yew Ann Leong, Kirthana Ganeshan, Jingwei Cai, Andrew D. Patterson, Peter J. Turnbaugh, Ajay Chawla

Issue&Volume: Volume 30 Issue 2

Abstract: Microbial dysbiosis and inflammation are implicated in diet-induced obesity and insulin resistance. However, it is not known whether crosstalk between immunity and microbiota also regulates metabolic homeostasis in healthy animals. Here, we report that genetic deletion of tuberous sclerosis 1 ( Tsc1) in CD11c + myeloid cells (Tsc1 f/fCD11c Cre mice) reduced food intake and body mass in the absence of metabolic disease. Co-housing and fecal transplant experiments revealed a dominant role for the healthy gut microbiota in regulation of body weight. 16S rRNA sequencing, selective culture, and reconstitution experiments further confirmed that selective deficiency of Lactobacillus johnsonii Q1-7 contributed to decreased food intake and body mass in Tsc1 f/fCD11c Cre mice. Mechanistically, activation of mTORC1 signaling in CD11c cells regulated production of L. johnsonii Q1-7-specific IgA, allowing for its stable colonization in the gut. Together, our findings reveal an unexpected transkingdom immune-microbiota feedback loop for homeostatic regulation of food intake and body mass in mammals.

DOI: https://doi.org/10.1016/j.cmet.2019.05.002

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(19)30242-6