研究人员描述了哺乳动物对膳食几丁质的适应，这种适应是由胃先天性免疫激活和酸性哺乳动物几丁质酶（AMCase）协调的。几丁质的摄入会导致小鼠胃部膨胀以及胃簇细胞和第2组先天性淋巴细胞（ILC2）产生细胞因子，从而推动表达AMCase的酶源性首领细胞的扩增，促进几丁质的消化。虽然几丁质会影响肠道微生物的组成，但无菌小鼠仍能保持ILC2介导的组织适应和胃肠道反应。在缺乏AMCase的情况下，持续摄入几丁质会导致基础2型免疫力增强、脂肪含量降低以及对肥胖的抵抗力增强。
这些数据定义了一种内源性代谢回路，它通过增强消化功能，从不溶性的膳食成分中提取营养物质。
据介绍，膳食纤维可改善代谢健康，但消化纤维多糖的宿主编码机制尚不清楚。
附：英文原文
Title: A type 2 immune circuit in the stomach controls mammalian adaptation to dietary chitin
Author: Do-Hyun Kim, Yilin Wang, Haerin Jung, Rachael L. Field, Xinya Zhang, Ta-Chiang Liu, Changqing Ma, James S. Fraser, Jonathan R. Brestoff, Steven J. Van Dyken
Issue&Volume: 2023-09-08
Abstract: Dietary fiber improves metabolic health, but host-encoded mechanisms for digesting fibrous polysaccharides are unclear. In this work, we describe a mammalian adaptation to dietary chitin that is coordinated by gastric innate immune activation and acidic mammalian chitinase (AMCase). Chitin consumption causes gastric distension and cytokine production by stomach tuft cells and group 2 innate lymphoid cells (ILC2s) in mice, which drives the expansion of AMCase-expressing zymogenic chief cells that facilitate chitin digestion. Although chitin influences gut microbial composition, ILC2-mediated tissue adaptation and gastrointestinal responses are preserved in germ-free mice. In the absence of AMCase, sustained chitin intake leads to heightened basal type 2 immunity, reduced adiposity, and resistance to obesity. These data define an endogenous metabolic circuit that enables nutrient extraction from an insoluble dietary constituent by enhancing digestive function.
DOI: add5649
Source: https://www.science.org/doi/full/10.1126/science.add5649