睡眠障碍影响长冠肺炎的炎症消退。

IF 3.2

Prostaglandins, leukotrienes, and essential fatty acids Pub Date : 2026-04-01 Epub Date: 2026-02-02 DOI:10.1016/j.plefa.2026.102728

Larissa C. Engert , Rammy Dang , Surya Daniel , Suzanne M. Bertisch , Jason H. Maley , Tamara G. Fong , Charles N. Serhan , Janet M. Mullington , Monika Haack

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引用次数: 0

摘要

背景：睡眠障碍是长冠肺炎的常见症状，可促进促炎状态，调节脂质衍生的特异性促炎介质（SPMs），可能导致慢性未解决炎症。本研究旨在探讨睡眠障碍在长COVID炎症消退中的作用。方法：我们研究了39名参与者（30F/9M，年龄22-68岁），其中31名长冠患者和8名未发生长冠的sars - cov -2感染对照。该研究包括14天的居家阶段，随后是1天（24小时）的实验室住院。使用PROMIS睡眠障碍t -评分评估睡眠障碍。在实验室停留期间，采集空腹晨血样本以评估脂质介质。数据分析采用广义线性混合模型。结果：长冠肺炎患者报告的睡眠障碍水平高于对照组（p2 (PGE2)）水平（pn-3 DPA (PD1n-3 DPA)），高于低睡眠障碍患者（t评分）。结论：本研究表明，睡眠障碍可能通过损害某些炎症消退途径，促进长冠肺炎患者的慢性炎症。促进炎症消退生理学，特别是在患有睡眠障碍的长冠状病毒患者中，可能是减轻长冠状病毒炎症和症状负担的机制靶点。试验注册：ClinicalTrials.gov NCT05606211。

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Sleep disturbance affects inflammatory resolution in Long COVID

Background

Sleep disturbance, which is a common symptom in Long COVID, promotes a pro-inflammatory state and dysregulates lipid-derived specialized pro-resolving mediators (SPMs), presumably contributing to chronic unresolved inflammation. This study aimed to investigate the role of sleep disturbance in inflammatory resolution in Long COVID.

Methods

We studied 39 participants (30F/9M, age range 22–68 years), including 31 individuals with Long COVID and 8 SARS-CoV-2-infected controls, who did not develop Long COVID. The study consisted of a 14-day at-home phase followed by a 1-day (24-h) in-laboratory stay. Sleep disturbance was assessed using PROMIS Sleep Disturbance T-scores. During the in-laboratory stay, a fasting morning blood sample was taken for assessment of lipid mediators. Data were analyzed using generalized linear mixed models.

Results

Participants with Long COVID reported higher sleep disturbance than controls (p<.001). Pro-inflammatory lipid pathways were upregulated in Long COVID compared to control, as indicated by higher prostaglandin E₂ (PGE₂) levels (p<.05). Long COVID participants with high sleep disturbance (PROMIS Sleep Disturbance T-score ≥60) had lower SPM levels, including the precursor of D-series resolvins 17-hydroxydocosahexaenoic acid (17-HDHA), 17R/S-resolvin D1 (17R/S-RvD1), 15R-lipoxin B4 (15R-LXB4), and protectin D1_{n-3 DPA} (PD1_{n-3 DPA}) than those with low sleep disturbance (T-score <60) (p<.05).

Conclusions

This study suggests that sleep disturbance may contribute to chronic inflammation in Long COVID by compromising certain inflammatory resolution pathways. Promoting inflammatory resolution physiology in particular in those individuals with Long COVID suffering from sleep disturbance may serve as a mechanistic target to mitigate inflammation and symptom burden in Long COVID.