小柯机器人

加拿大多伦多大学Tae-Hee Kim研究组发现在出生后发育早期，肠道菌群通过巨噬细胞和间充质龛促进干细胞分化。这一研究成果发表在2022年12月5日出版的国际学术期刊《免疫》上。

他们研究了早期生命微生物接触和这一过程的破坏如何影响肠干细胞的生态位和发育。单细胞转录分析显示，早期抗生素治疗后，干细胞分化为Paneth细胞和巨噬细胞特化受损。小鼠遗传和类器官共培养实验表明，CD206+肠道巨噬细胞亚群分泌Wnt配体，维持了对Paneth细胞分化重要的间充质龛细胞。抗生素和Paneth细胞数量减少与致命的婴儿疾病，坏死性小肠结肠炎(NEC)有关。他们发现，乳酸菌定植或CD206+巨噬细胞转移促进Paneth细胞分化，降低NEC的严重程度。总之，他们的工作确定了在出生后早期发育中肠道微生物群介导的干细胞龛调节。

据悉，肠道干细胞的成熟发育与出生后肠道菌群接触相吻合。

附：英文原文

Title: Gut microbiota promotes stem cell differentiation through macrophage and mesenchymal niches in early postnatal development

Author: Ji-Eun Kim, Bo Li, Lijiang Fei, Rachael Horne, Dorothy Lee, Adrian Kwan Loe, Hiromu Miyake, Eda Ayar, Dae-Kyum Kim, Michael G. Surette, Dana J. Philpott, Philip Sherman, Guoji Guo, Agostino Pierro, Tae-Hee Kim

Issue&Volume: 2022-12-05

Abstract: Intestinal stem cell maturation and development coincide with gut microbiota exposureafter birth. Here, we investigated how early life microbial exposure, and disruptionof this process, impacts the intestinal stem cell niche and development. Single-celltranscriptional analysis revealed impaired stem cell differentiation into Paneth cellsand macrophage specification upon antibiotic treatment in early life. Mouse geneticand organoid co-culture experiments demonstrated that a CD206+ subset of intestinal macrophages secreted Wnt ligands, which maintained the mesenchymalniche cells important for Paneth cell differentiation. Antibiotics and reduced numbersof Paneth cells are associated with the deadly infant disease, necrotizing enterocolitis(NEC). We showed that colonization with Lactobacillus or transfer of CD206+ macrophages promoted Paneth cell differentiation and reduced NEC severity. Together,our work defines the gut microbiota-mediated regulation of stem cell niches duringearly postnatal development.

DOI: 10.1016/j.immuni.2022.11.003

Source: https://www.cell.com/immunity/fulltext/S1074-7613(22)00593-3

Immunity：《免疫》，创刊于1994年。隶属于细胞出版社，最新IF：43.474
官方网址：https://www.cell.com/immunity/home
投稿链接：https://www.editorialmanager.com/immunity/default.aspx