Diya Nikki, Pierce Mercedes I, Bhatt Shantanu, Nelson Matthew D
Biology, Saint Joseph's University, Philadelphia, Pennsylvania, United States.
MicroPubl Biol. 2025 Aug 7;2025. doi: 10.17912/micropub.biology.001738. eCollection 2025.
Stress-induced sleep of occurs following exposure to noxious stressors, such as pore forming toxins, extreme temperature, ultraviolet irradiation, tissue wounding, and viral infections. Enteropathogenic (EPEC) is a pathogenic bacterium which can infect , however stress-induced sleep in response to EPEC has not been investigated. EPEC affects worms via two distinct mechanisms: 1) Contact-independent paralysis which occurs following the release of the toxin indole; 2) Contact-dependent bacterial colonization of the intestine. Here we examine mechanism one; we find that indole induced paralysis is regulated independently of the ALA and RIS sleep neurons. In fact, impairing ALA and RIS function caused animals to paralyze significantly faster than controls. Increasing cholinergic or GABAergic input, accelerated or delayed paralysis, respectively. Worms exposed to indole who were subsequently rescued to normal growth plates displayed a compensatory stress-induced sleep that was RIS but not ALA dependent. This work will allow for detailed future investigations into indole's mechanism of action, EPEC pathogenicity, and how bacterial infection leads to recovery sleep.
应激诱导睡眠发生在暴露于有害应激源之后，如成孔毒素、极端温度、紫外线照射、组织损伤和病毒感染。肠致病性大肠杆菌（EPEC）是一种可感染[具体生物]的致病细菌，然而，尚未对EPEC诱导的应激诱导睡眠进行研究。EPEC通过两种不同机制影响蠕虫：1）毒素吲哚释放后发生的非接触性麻痹；2）肠道的接触依赖性细菌定植。在此，我们研究机制一；我们发现吲哚诱导的麻痹独立于ALA和RIS睡眠神经元进行调节。事实上，损害ALA和RIS功能会导致动物比对照组更快地麻痹。增加胆碱能或GABA能输入，分别加速或延迟麻痹。暴露于吲哚后被转移到正常生长平板上的蠕虫表现出一种补偿性应激诱导睡眠，这种睡眠依赖于RIS而非ALA。这项工作将为未来详细研究吲哚的作用机制、EPEC致病性以及细菌感染如何导致恢复性睡眠提供可能。
