Xu Qianqian, Lv Mengqi, Yuan Yiwei, Ling Tianliang, Zou Xiaoting, Dong Xinyang
Key Laboratory of Characteristic Agricultural Product Quality and Hazardous Substance Control Technology of Zhejiang Province, Institute of Food Nutrition and Quality Safety, College of Life Science, China Jiliang University, Hangzhou, 310018, China; Key laboratory for Molecular Animal Nutrition of Ministry of Education, Key Laboratory of Animal Feed and Nutrition of Zhejiang Province, Feed Science Institute, College of Animal Science, Zhejiang University (Zijingang Campus), Hangzhou, 310058, China.
Key Laboratory of Characteristic Agricultural Product Quality and Hazardous Substance Control Technology of Zhejiang Province, Institute of Food Nutrition and Quality Safety, College of Life Science, China Jiliang University, Hangzhou, 310018, China.
Poult Sci. 2024 Dec;103(12):104243. doi: 10.1016/j.psj.2024.104243. Epub 2024 Aug 22.
Stress damage caused by early weaning and its possible mechanism have been studied mainly in young mammals, but rarely in altrices, especially in squabs. The study aimed to investigate the possible molecular mechanism of intestinal epithelial barrier damage caused by early weaning in squabs through determining the intestinal permeability, the ultrastructure of villous epithelium, the contents of ileal cytokines, and the protein relative expression of tight-junction proteins, TLRs and their mediated key factors in inflammatory signaling pathways. A total of 192 newly hatched squabs were randomly divided into 2 groups, 1 group was weaned and fed artificial pigeon milk from d 7, and the other group continued to be fed by the parent pigeons. The ileal mucosa and serum of 8 replicates were collected at 1, 4, 7, 10, and 14 d after weaning. The results indicated that early weaning could reduce the growth performance of squabs and damage the intestinal epithelial barrier, which is characterized by down-regulating the protein expression of claudin-1/3, up-regulating the protein expression of claudin-2, promoting the secretion of pro-inflammatory factors, inhibiting the secretion of anti-inflammatory factors, and increasing the permeability of the intestinal barrier. The specific mechanism of stress damage might be the activation of TLR2/4-MyD88-ERK/JNK inflammatory signaling pathway leading to the increase levels of IL-6 and TNF-α.
早期断奶引起的应激损伤及其可能机制主要在幼年哺乳动物中进行了研究，但在晚成雏中研究较少，尤其是在雏鸽中。本研究旨在通过测定雏鸽肠道通透性、绒毛上皮超微结构、回肠细胞因子含量以及紧密连接蛋白、Toll样受体（TLRs）及其介导的炎症信号通路关键因子的蛋白相对表达，探讨早期断奶引起雏鸽肠道上皮屏障损伤的可能分子机制。将192只新孵出的雏鸽随机分为2组，一组从第7天开始断奶并喂人工鸽乳，另一组继续由亲鸽喂养。在断奶后第1、4、7、10和14天收集8个重复样本的回肠黏膜和血清。结果表明，早期断奶会降低雏鸽的生长性能并损害肠道上皮屏障，其特征为下调claudin-1/3蛋白表达、上调claudin-2蛋白表达、促进促炎因子分泌、抑制抗炎因子分泌以及增加肠道屏障通透性。应激损伤的具体机制可能是TLR2/4-MyD88-ERK/JNK炎症信号通路的激活导致IL-6和TNF-α水平升高。
