摘要
      耐多药细菌，尤其是病原体，对疾病的治疗和恢复构成严重威胁，但它们对动物发育的潜在毒性尚不完全清楚。作为营养吸收最重要的部位，我们通过分析耐多药志贺菌对热带爪蟾肠道健康的影响，研究了热带爪蟾的肠道微生物组。与对照组不同，志贺菌的摄入促进了中性粘液的分泌，抑制了肠道发育和体重增加。暴露60天后，观察到肠隐窝萎缩、肠绒毛缩短、内腔扩大和外粘膜肌肉崩解。肠道环肌和纵肌随着病原体暴露量的增加而变薄。此外，志贺菌的存在改变了肠道中多种细胞因子的表达和经典的抗氧化酶活性，这可能导致了我们观察到的肠道损伤。肠道样本的16S rDNA测序分析表明，接触志贺菌破坏了正常肠道微生物的丰度和多样性，并增加了功能性细菌的比例。值得注意的是，肠道抗生素耐药性基因（ARGs）丰度的增加可能意味着志贺菌携带的耐药性基因很容易在肠道内迁移和传播。我们的研究结果扩展了关于耐多药志贺菌诱导热带X.热带X.肠道毒性的现有知识，并为耐药病原体携带的耐药基因的威胁评估提供了新的见解。
Abstract
Multidrug-resistant bacteria, especially pathogens, pose a serious threat to disease treatment and recovery, but their potential toxicity to animal development is not entirely clear. As the most important site for nutrient absorption, we studied the intestinal microbiome of Xenopus tropicalis by analyzing the effect of multidrug-resistant Shigella on its intestinal health. Unlike in the control, Shigella intake promoted the secretion of neutral mucus and inhibited intestinal development and weight gain. Following 60 days of exposure, intestinal crypt atrophy, intestinal villus shortening, internal cavity enlargement, and external mucosal muscle disintegration were observed. The circular and longitudinal intestinal muscles became thinner with increasing pathogen exposure. In addition, the presence of Shigella altered the expression of multiple cytokines and classic antioxidant enzyme activities in the gut, which may have caused the intestinal lesions that we observed. 16 S rDNA sequencing analysis of intestinal samples showed that exposure to Shigella destroyed the normal gut microbial abundance and diversity and increased the functional bacterial ratio. Notably, the increased abundance of intestinal antibiotic resistance genes (ARGs) may imply that the resistance genes carried by Shigella easily migrate and transmit within the intestine. Our results expand existing knowledge concerning multidrug-resistant Shigella-induced intestinal toxicity in X. tropicalis and provide new insights for the threat assessment of resistance genes carried by drug-resistant pathogens.

https://www.sciencedirect.com/science/article/pii/S0269749122017651