Engert et al. (2026)
- Authors: Larissa C. Engert, Rammy Dang, Surya Daniel, Suzanne M. Bertisch, Jason H. Maley, Tamara G. Fong, Charles N. Serhan, Janet M. Mullington, Monika Haack
- Institutes: Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA, USA, Division of Sleep Medicine, Harvard Medical School, Boston, MA, USA, Division of Sleep and Circadian Disorders, Brigham and Women’s Hospital, Boston, MA, USA, Aging Brain Center, Marcus Institute for Aging Research, Hebrew SeniorLife, Boston, MA, USA, Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women’s Hospital, Boston, MA, USA
- Publisher: Prostaglandins, Leukotrienes and Essential Fatty Acids
- Link: DOI
Summary
This study provides critical evidence that sleep disturbance in Long COVID patients is linked to a failure in the body’s natural inflammatory resolution process. By identifying reduced levels of specialized pro-resolving mediators, the research suggests that sleep management could be a key therapeutic target to reduce chronic inflammation and improve recovery.
What was researched?
The study investigated the impact of sleep disturbance on the levels of lipid-derived specialized pro-resolving mediators (SPMs) 💊 in patients with Long COVID.
Why was it researched?
Sleep disturbance is a hallmark symptom of Long COVID and is known to promote inflammation, so researchers hypothesized it might prevent the body from successfully resolving the inflammatory response.
How was it researched?
A cohort of 31 Long COVID patients and 8 controls was assessed for sleep quality and blood concentrations of pro-inflammatory markers and SPMs using mass spectrometry.
What has been found?
Long COVID patients with high sleep disturbance had significantly lower levels of key SPMs, including 17-HDHA and Resolvin D1, compared to those with better sleep. Additionally, the pro-inflammatory marker PGE2 was elevated in Long COVID participants.
Discussion
The findings suggest that sleep-related deficits in resolution molecules may drive persistent inflammation. Limitations include the small sample size and observational nature, which prevents establishing a direct cause-and-effect relationship.
Conclusion & Future Work
Sleep disturbance appears to impair the physiology of inflammatory resolution in Long COVID. Enhancing sleep quality or pharmacologically supporting SPM pathways could offer a new mechanistic target for symptom mitigation.