Yi Lingxian, Ren Zining, Feng Yu, Zhang Yechun, Liu Jianshuo, Yuan Xiaowu, Kuang Qihong, Deng Hui, Yang Bo, Yu Daojin
Fujian Key Laboratory of Traditional Chinese Veterinary Medicine and Animal Health, College of Animal Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
Antibiotics (Basel). 2025 Apr 30;14(5):460. doi: 10.3390/antibiotics14050460.
The impact of heat stress on intestinal bacterial antimicrobial resistance (AMR) and its underlying mechanisms is not fully understood. This study aims to explore how heat stress influences AMR in the gut and the mechanisms involved.
A Specific-Pathogen-Free (SPF) mouse model was used, divided into a control group (maintained at 25 °C) and a heat stress group (exposed to 42 °C for 30 min twice daily for 55 days). The effectiveness of the model was verified by RT-qPCR and histopathological analysis. Antibiotic susceptibility testing and clonal analysis (ERIC-PCR) were performed. Colonization assays were conducted to determine the accumulation of resistant strains in the gut. Metagenomic sequencing was conducted to investigated microbial composition.
RT-qPCR and Histopathological analysis revealed intestinal damage and significant upregulation of genes related to stress response, intestinal barrier integrity and inflammation, indicating successful model establishment and physiological alterations. Antibiotic susceptibility testing revealed increased resistance to erythromycin, chloramphenicol, and tetracycline among strains. Clonal analysis demonstrated that these resistant strains were clonally unrelated. Sequencing identified a novel -carrying integrative and conjugative element (ICE) among four erythromycin-resistant strains. The rectum harbored a higher proportion of erythromycin-resistant strains with elevated minimum inhibitory concentrations (MICs) after 25 days of heat stress exposure. Colonization assays confirmed that heat stress led to the accumulation of erythromycin-resistant in the rectum. Metagenomic sequencing revealed significant changes in microbial composition, favoring anaerobic metabolism.
This study suggests that chronic heat stress can promote the emergence of antibiotic-resistant strains through ICE transfer, providing insight for environmental safety.
热应激对肠道细菌抗菌耐药性（AMR）的影响及其潜在机制尚未完全明确。本研究旨在探讨热应激如何影响肠道中的AMR及其相关机制。
使用无特定病原体（SPF）小鼠模型，分为对照组（维持在25°C）和热应激组（每天两次暴露于42°C，持续30分钟，共55天）。通过RT-qPCR和组织病理学分析验证模型的有效性。进行抗生素敏感性测试和克隆分析（ERIC-PCR）。进行定植试验以确定耐药菌株在肠道中的积累。进行宏基因组测序以研究微生物组成。
RT-qPCR和组织病理学分析显示肠道损伤以及与应激反应、肠道屏障完整性和炎症相关的基因显著上调，表明模型建立成功且发生了生理改变。抗生素敏感性测试显示菌株对红霉素、氯霉素和四环素的耐药性增加。克隆分析表明这些耐药菌株在克隆上无关联。测序在四株耐红霉素菌株中鉴定出一种携带新型整合和接合元件（ICE）。热应激暴露25天后，直肠中耐红霉素菌株的比例更高，最低抑菌浓度（MIC）升高。定植试验证实热应激导致直肠中耐红霉素菌的积累。宏基因组测序显示微生物组成发生显著变化，有利于厌氧代谢。
本研究表明，慢性热应激可通过ICE转移促进抗生素耐药菌株的出现，为环境安全提供了见解。
