研究组报道，在发育中的斑马鱼中，肠内分泌细胞在淋巴细胞填充肠道之前响应微生物信号产生白细胞介素-22 （IL-22）。在幼虫中，IL-22塑造肠道菌群，增加乳酸杆菌科的丰度和ghrelin的表达，促进肠道蠕动。运动障碍和胃饥饿素的表达在il22 /通过从野生型斑马鱼转移微生物群或仅引入植物乳杆菌来获得斑马鱼。IL-22缺陷小鼠在生命早期也有肠道运动受损和胃饥饿素表达减少，表明其功能保守。在免疫系统成熟之前，肠内分泌细胞通过IL-22控制微生物群来调节早期肠道功能。
研究人员表示，肠道菌群、免疫系统和肠神经系统相互作用，调节成人肠道生理。然而，在发育过程中建立肠道生理的机制仍然未知。
附：英文原文
Title: IL-22 from enteroendocrine cells promotes early-life gut motility in zebrafish through the microbiota
Author: Soraya Rabahi, Lucie Maurin, Emiliano Marachlian, Fabian Guendel, Aya Mikdache, Keinis Quintero-Castillo, Vincenzo Di Donato, Jessica Riou-Ramon, Akshai Janardhana Kurup, Yazan Salloum, Gwendoline Gros, Patricia Diabangouaya, Camila Garcia-Baudino, Ignacio Medina-Yáez, Pascal Hersen, Alvaro Banderas, Jean-Pierre Levraud, Georges Lutfalla, Filippo Del Bene, Carmen G. Feijoo, Gerard Eberl, German Sumbre, Jos Boekhorst, Sylvia Brugman, Pedro P. Hernandez
Issue&Volume: 2026-04-02
Abstract: The gut microbiota, immune system, and enteric nervous system interact to regulate adult gut physiology. However, the mechanisms establishing gut physiology during development remain unknown. We report that in developing zebrafish, enteroendocrine cells produced interleukin-22 (IL-22) in response to microbial signals before lymphocytes populated the gut. In larvae, IL-22 shaped the gut microbiota, increasing Lactobacillaceae abundance and ghrelin expression to promote gut motility. Impaired motility and ghrelin expression were restored in il22/ zebrafish by transfer of microbiota from wild-type zebrafish or by introducing only Lactobacillus plantarum. IL-22–deficient mice also had impaired gut motility and reduced ghrelin expression in early life, indicating a conserved function. Thus, before immune system maturation, enteroendocrine cells regulate early-life gut function by controlling the microbiota through IL-22.
DOI: adr1707
Source: https://www.science.org/doi/10.1126/science.adr1707